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444 Cards in this Set
- Front
- Back
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Henderson-Hasselbach equation
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pH = pKa + log ((A-)\(HA))
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When is the buffer capacity highest?
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when pH = pKa
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1 kcal = x kJ?
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1.4 kJ
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aromatic AAs
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tyrosine, tryptophan, phenylalanine
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D- or L- saccharides are important in nature?
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D-monosaccharides
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anomer
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cyclic stereoisomerism (mutarotation) (used for saccharides), alpha and beta
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epimer
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isomers of saccharides differing in orientation of one -OH group in space
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mannose
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2-epimer of Glc
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Gal
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4-epimer of Glc
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reducing sugar
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any sugar that form carbonyl group (hemiacetal) (=sucrose is not)
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cellulose
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βGlc(1→4)Glc
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Inulin, what, source
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Frc β(2→1) (can have terminal glucose), fructan fiber found in plants
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coagulation factors acted on by gamma-glutamyl carboxylase
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2,7,9,10
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Vitamin B1/Thiamine, deficiency-related disorder
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1 Beriberi (SEA - processed rice, symptoms - wet beriberi = high-output cardiac failure, dry beriberi = peripheral neuropathy) 2 Wernicke-Korsakoff encephalopathy (ataxia, memory loss - pathonomic = confabulous (make up stories about past events and believes it, breakdown of brain tissue, malnutrition in long-term alcoholism)
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Vitamin B1/Thiamine, function
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TDP/TPP(Thiamine pyro/diphosphate) is co-factor for several enzymes - transketolase (PPP), alpha-ketoacid decarboxylation (PDH, alphaketoglutarate DH)
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Vitamin B2/Riboflavin, deficiency-linked disorder, characteristic
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3 mouth disorders - angular stomatitis/cheilitis (inflammation and fissuring radiating from the commissures of the mouth), glossitis, cheilitis (inflammation of lips)
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Vitamin B2/Riboflavin, function
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form the co-factors FMN (flavin mononucleotide) (complex I) and FAD (flavin adenine dinucleotide) (complex II) (both are not nucleotides because sugar is ribitol not ribose
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Vitamin B3/Niacin, deficiency-linked disorder
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Pellegra - ''maize diet'' (central and south american indians), 3Ds - diarrhea, dementia, dermatitis (by hartnup disease)
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Vitamin B3/Niacin/Nicotinic acid - function
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form co-factors NAD (nicotinamide dinucleotide) (catabolism) and NADP (anabolism (FA, cholesterol))
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Vitamin B3/Niacin/Nicotinic acid, source
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endogenous - from Trp (Trp -> kynurenine -> Niacin)
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Vitamin B5/Pantothenic acid, function
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in co-factors CoA and ACP (acyl-carrier protein, FA synthesis, not really cofactor)
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Vitamin B6/Pyridoxine, function
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co-factor pyridoxal phosphate (PLP) (oxidized pyridoxine which is alcohol) - 1 transaminases (form schiff base) 2 glycogen phosphorylase (unknown function) 3 glutamic acid decarboxylase (glutamate to GABA) 4 some deaminations
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Vitamin D/Cholecalciferol (calciol), source
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7-dehydroxycholesterol –(UV)-> cholecalciferol\calciol –(25-hydroxylase, liver)-> ergocalciferol/calcifediol\25-hydroxycholecalciferol (low activity) –(1-α-hydroxylase, kidney, control point)-> calcitriol\1,25-dihydroxycholecalciferol (high activity)
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Vitamin D/cholecalciferol, main effect
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hypercalcemic in intestine (VDR in nucleus, gene regulatory complex, calbindin++) and to a lesser degree in kidney, hyperphosphatemic in intestine and kidney (inhibit excretion)
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Vitamin K - function
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co-factor for gamma glutamyl carboxylase (double carboxylate glutamate at Cgamma, so coagulation factors can bind to Ca2+, one of few carboxylase which don't use biotin)
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Vitamin K, vitamin B7/H/Biotin, and vitamin B12/Cobalamin- source
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intestinal bacteria (and ingested bacteria)
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vitamin K-associated deficiency disorder - cause, signs
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newborns (underdeveloped GI flora), hemoorrhage
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Warfarin - effect
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vitamin K antagonist (by inhibiting vitamin K epoxide reductase (recycles oxidized vitamin K to its reduced form after it has carboxylated))
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1-2?
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1 nicotinamide 2 Nicotinamide adenine dinucleotide phosphate (NADP+) (NAD+ lack Pi on 2 of adenosine)
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?
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flavin mononucleotide (FMN)/Riboflavin-5'-phosphate
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?
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FADH2 (sugar of flavin is ribitol so its not technically a nucleotide, link is C-N not C-O-N (glycosidic)) (the two Hs is attached to the 2 free Ns of flavin)
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?
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Thiamine
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?
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TDP/TPP (Thiamine pyrophosphate)
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?
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Ascorbic acid
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aryl
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an organic radical derived from an aromatic compound by removing a hydrogen atom
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compound?
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Riboflavin/B2
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excessive vitamin D intake is linked to
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1 hypercalcemia 2 hypercalcification of soft tissue 3 stupor 4 inability to eat
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imines 1 aldimine - primary and secondary 2 ketimines - primary and scondary
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1 primary aldimine = C(R)(H)=NH, secondary aldimine C(R)(H)=NR'' 2 primary ketimine C(R')(R'')=NH, secondary ketimine C(R')(R'')=N-R'''
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Schiff base, used by which enzymes (2)
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condensation product of aldehyde/ketone w a primary amine (one C) form a secondary imine/schiff base which is C(R')(H/R'')=N(R''/R'''), 1 transaminases (pyridoxine) 2 aldolase
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Vitamin A deficiency - signs & symptoms
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1 Night blindness 2 Skin disorders 3 Improper bone formation 4 Inadequate tooth enamel
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vitamin B6/pyridoxine, deficiency-related disorder
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pyridoxine deficiency - neurological = peripheral neuropathy (sensory), scaly dermatitis, anemia
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Vitamin D deficiency related disorders
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1 Rickets (children) 2 Osteomalacia (adults) 3 melanona (epidemiological linkage)
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Vitamin H/biotin/vitamin B7, deficiency-linked disorder
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due to raw egg white diet (the thermolabile protein avidin bind biotin, need 20 egg whites/day) - neurological (depression, lethargy), conjunctivitis, dermatitis
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Vitamin H/Vitamin B7/Biotin, function
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cofactor for most carboxylase reactions (pyruvate carboxylase, PEP carboxylase, acetyl-CoA carboxylase, Propionyl-CoA carboxylase)
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beta oxidation, repetitive process
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1 oxidation (acyl CoA DH, FAD) 2 hydration (enoyl CoA hydratase, = beta-hydroxyacyl CoA) 3 oxidation (beta-hydroxy acyl CoA DH, = beta-keto acyl CoA) 4 thiolysis (beta-ketothiolase = fatty acyl CoA + acetyl CoA
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effect of binding of xenobiotics on excretion time
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decreased - can only act on free substances
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fatty acid synthesis - repetitive process
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1 condensation (acetyl + malonyl, malonyl decarboxylates = beta-ketoacyl) 2 reduction (NADPH, = beta-hydroxyacyl) 3 dehydration (produce double bond between C2-C3) 4 reduction (double bond is reduced by NADPH = four-carbon acyl)
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folate - deficiency-linked disorder
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1 megaloblastic anemia (due to arrest of DNA synthsis in rapidly dividing cells) 2 neurotubule defects (spina bifida) (both defects are due to folate being able to carry many types of one-carbons (formyl, methyl, methylene), but methyl group can only be removed by b12, methylene-tetrahydrofolate is needed to make thymidine)
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folate, function
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dihydrofolate reductase (inhibit by methotrexate) reduce it to the co-factor tetrahydrofolate (THF), function as one-carbon donor (from serine, glycine, formaldehyde, histidine, to dUMP (becomes dTMP) and in purine synthesis)
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In what 4 ways are pyridoxine needed in the body? (not at biochemical level)
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1 antibodies 2 hemoglobin 3 utilization of copper 4 utilization of iron
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lipoic acid, involved in which reactions?
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oxidation of the keto group of a decarboxylated alpha-ketoacid
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testosterones - number of Cs of 1 cholestanes (cholesterol) 2 cholanes (cholic acid) 3 pregnanes (progesterone) 4 androstanes (testosterone) 5 estranes (estradiol)
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1 27 2 24 3 21 4 19 5 18
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vitamin B12/cobalamin, function
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co-factor for 2 enzymes - 1 methyl-malonyl CoA mutase (MUT) (propionyl CoA accumulation in brain = neurological symptoms) (co-factor = adenosylcobalamin) 2 5-methyltetrahydrofolate-homocysteine methyl transferase MTR): homocysteine -> methionine (co-factor = methylcobalamin) (deficiency “traps” THF as 5-methyl-folate)
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vitamin B12/Cobalamin, structure
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cobalt in a ring that resemble porphyrin
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vitamin B12/cobalamin-deficiency linked disorder
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cause a functional deficiency of folate (megaloblastic anemia, spinal cord abnormalities), linked to lack of intrinsic factor
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vitamin C - function
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1 hydroxylation reactions (proline and lysine for collagen) 2 absorption of iron facilitator 3 antioxidant
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vitamin C-linked deficiency disorder
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Scurvy - easy bruising, muscular fatigue, hemorrhage and anemia
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Vitamin E, functions
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1 Protect against hemolysis 2 Aid in rbc production 3 Support liver and muscle function (4 cardioprotective in high doses)
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Vitamin E/Tocopherol - mechanism behind its cardioprotective effect
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vitamin E/tocopherols in high doses (above 2500 units/day) is shown to be cardioprotective in some research (hypothesis = vit D is carried in LDL and help prevent oxidation of LDL particles, main negative effect of LDL is through oxidized particles, must take high dose vitamin C also to recycle oxidized vit E)
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albumin binds
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1 FFAs 2 Drugs 3 Non-conjugated bilirubin (Gilbert sy) 4 Hormones 5 Some fat-soluble vitamins 6 Ca2+
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cytochrome P450 - characteristics
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1 important polymorphism (warfarin) 2 broad/low substrate specificity 3 most are inducible (u transcriptional level)
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cytochrome P450 - location
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hemoproteins in membrane of SER or inner mitochondrial membrane, most abundant in 1 liver 2 small intestine 3 lungs (also involved in biosynthesis of steroids, bile acids, eicosanoids and unsaturated FAs) 4 skin
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Cytochrome P450 family - nomenclature (use CYP3A4)
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CYP = cytochrome P450, 3 = family, A = subfamily (based on AA-sequence), 4 = isoform
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cytochrome P450 system - mechanism
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isoenzyme family of a 60, monoxygenase, receive electrons from NADPH-cytochrome P450 reductase and transfer them to FAD for reduction of molecular oxygen (create superoxide) to incorporate it into the substrate
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drugs - example of polar and nonpolar
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polar = amiodarone, phentanyl (transdermal uptake), non-polar = penicillin
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enzyme/reaction of phase I/biotransformation phase of xenobiotic metabolism
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1 hydrolases (esterases, peptidases) 2 Cytochrome P450 system (CYP450 family of co-factor)/mixed function oxidase(MFO)(describe their broad specificity)/Monooxygenases (describe their mechanism) 3 deamination, dealkylation 4 amidation 5 carboxylation
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how is paracetamol and aflatoxins hepatotoxic?
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1st biotransformation reaction create radical. Its hepatoxic by depleting NADPH (CYP450) which result in ability to neutralize radicals and necrosis
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metabolism of xenobiotics can cause
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1 lowered toxicity 2 increased toxicity 3 bioactivation 4 increasing their water solubility
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mixed function oxygenase (MFO)
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any monooxygenase that catalyzes AH + O2 + DH2 -> AOH + H2O + D
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phase I, biotransformation of xenobiotics, location
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ER-membranes and cytoplasm, primary liver also lungs, intestine, skin and kidneys
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phases of metabolism of xenobiotics
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1 biotransformation (create polar functional groups) 2 conjugation (polar endogenic compounds is attached)
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reactions of phase I of xenobiotic metabolism
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1 hydrolysis 2 oxidation (hydroxylation, epoxidation) 3 oxidative cleavage (dealkylation, deamination) 3 reduction 4 methylation
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simplifed reaction of CYP450 system
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o R-H + O2 + NADPH + H+ -> R-OH + H2O + NADP+ (FAD as intermediate electron transporter, create superoxide)
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which substances can be epoxidized? by which enzyme?
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aryls (aromatic compounds) and alkenes (less frequently), CYP450 system
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acetylsalicylic acid (cyclooxygenase inhibitor), degradation
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1 ester bond is hydrolyzed (intestine, blood) 2 conjugate w glycine = salicyluric acid
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aflatoxin b1 (aromatic 5-ring compound) - carcinogenic effect
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its biotransformed carcinogenic epoxide forms guanine adduct
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conjugate endogenic substrates and their active form
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1 glucuronic acid (UDP-glucuronate) 2 sulfate (PAPS (3-phosphoadenosine-5-phosphosulfate)) 3 acetate (Acetyl CoA) 4 Cysteine (Glutathione) 5 CH3 (SAM) 6 Gly, Glu (amidation)
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Cytochrome P450 system - most active enzyme
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CYP3A4
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degradation of glutathione-conjugated compound (bound to S of cysteine)
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1 glutamyl (gamma-glutamyl-transpeptidase) and glycinyl (dipeptidase) is removed 2 acetyl added to amine of cysteine (N-acetyltransferase) 3 mercapturic acid is excreted
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how is atherosclerosis linked to alcoholism?
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↑ synthesis of FAs and Cholesterol (↑acetyl CoA substrate) -> ↑VLDL and LDL
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how is liver cirrhosis (loss of structural arrangement) caused by alcoholism?
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via liver steatosis (↑TAG <- ↓VLDL <- ↓protein <- malnutrition) and then liver fibrosis, by ROS-induced necrosis (depleted NADPH)
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main enzyme which degrades catecholamines? mechanism?
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Catechol O-methyl transferase (COMT), introduce a methyl group from SAM
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methanol - toxic and lethal dose
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5-10 mL, 30 mL
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methanol - why is it toxic? cause of death?
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toxic due to formic acid (strongest organic acid), die of metabolic acidosis (loss of sight due to formic acids toxic effect on the optic nerve)
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pharmacodynamics of ethanol
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90% is metabolized (as energy, not gluconeogenic), 10% excreted (urine, breath, perspiration)
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which 3 compounds is absorbed in the stomach?
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1 Ethanol 2 Water (aquaporins) 3 SCFAs (short-chain FAs)
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which compounds is conjugated by GSH?
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electrophilic xenobiotics - ie drugs and carcinogens (which could otherwise form adducts)
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which enzyme can degrade/neutralize a carincogenic epoxide (located in ER)
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epoxide hydrolase (create diols)
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which substances can be conjugated by sulfation?
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1 some alcohols 2 arylamines 3 phenols 4 steroids 5 glycolipids 6 glycoproteins
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ammonia for urea cycle - produced by
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1 glutaminase 2 glutamate DH 3 from aspartate (deamination) 4 catabolism of Ser, Thr, His 5 intestinal bacteria
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chondroitin 6-sulfate
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glucuronic acid beta (1,3) N-acetylgalactosamine (6S)
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Crigler-Najjar
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severe congenital jaundice due to mutation of UDP-glucuronosyl-transferase
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Fischer projection, arrow? dotted arrow?
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arrow = against, dotted arrow = away from
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Gilbert syndrome
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decreased activity of UDP-glucuronosyl-transferase (UGT), benign, ''stress''-induced jaundice
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glutaminase in the kidney, use of product?
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ammonia is excreted in the urine to bind to H+
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heparin
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glucuronic acid (2S) alpha (1,4) glucosamine (2S,6S)
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hyaluronan
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glucuronic acid beta (1,3) n-acetylglucosamine
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keratan sulfate
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galactose alpha (1,4) N-acetylglucosamine (6S)
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Leigh syndrome, affect which enzyme complex?
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complex II/succinate DH/succinate/co-Q reductase (SQR) (cause encephalopathy)
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LHON (Leber's hereditary optic neuropathy), affect which enzyme complex?
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complex I/NADH dehydrogenase/NADH
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MELAS (mitochondrial encepahalopathy, lactic acidosis and stroke-like episodes), affect which enzyme complex?
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complex I/NADH dehydrogenase/NADH
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reactive nitrogen species (RNS)
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1 nitric oxide (NO*) 2 peroxynitrite (OONO-)(not free radical, but still very reactive)
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reactive oxygen species, which
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1 oxygen/O2** (biradical = 2 unpaired electrons) 2 superoxide/O2-* (oxygen + 1e-) 3 peroxide (O22-) (not a free radical, but very reactive) 4 hydroxyl radical (OH-*)(most reactive)
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source of free radicals
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1 neutrophils and macrophages (superoxide) 2 NO synthase (signaling, leukocytes) 3 ionizing radiation (create hydroxyl radicals) 4 electron transport chain (I, III, glycerol phosphate DH) 5 ferrous ion (2+) oxidation
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ascorbic acid - mechanism as antioxidant
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aromatic hydrophilic ring, when its transformed into a free radical its simply excreted (ie reduce ferrous ion (3+) and cuprous ion)
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damage of lipids by free radicals
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1 free radical take a H+ from a single bond between two double bonds of a unsaturated FA 2 fatty acid = fatty acid radical at C 3 fatty acid radical at C + oxygen = peroxyl radical 4 peroxyl radical take H+ from neighboring FA = FA peroxide + new peroxyl radical
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dismutation
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type of reaction where two molecules of the same compound react together to form one oxidized and one reduced form
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Incretins, what? which?
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GI hormones that cause an increase in insulin release after eating before blood glucose levels become elevated, GLP-1 (glucagon-like polypeptide 1) and GIP (gastric inhibitory peptide)
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metabolic pathways in SER
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1 TAG & PL synthesis 2 elongation and desaturation of FAs 3 steroid synthesis 4 biotransformation of xenobiotics 5 Glu-6Pase
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metabolic pathways in the cytosol?
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1 glycolysis 2 glycogenesis & lysis (liver & muscle) 3 pentose cycle 4 fatty acid synthesis 5 non-essential AA synthesis 6 transamination reaction 7 purine and pyrimidine metabolism 8 gluconeogenesis (from OAA or glycerol) (9 part of 1 urea synthesis (liver) 2 heme synthesis)
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metabolic pathways in the mitochondria
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1 PDH complex 2 beta oxidation 3 ketone body synthesis (liver) 4 oxidative deamination of glutamate 5 transaminations 6 citrate cycle (matrix) 7 resp chain (inner mitochondrial membrane) 8 aerobic phosphorylation (Fo F1 ATPase)(inner mitochondrial membrane) (9 part of 1 gluconeogenesis 2 heme synthesis 3 urea synthesis (liver))
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most susceptible groups of AAs to free radical damage, what?
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cysteine (due to thiol group) (form thiol radical = thiyl -> disulfide, sulfinic acid (hydroxyradical + (-SOH))
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NAs, damage of NAs
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1 damage at base (attach radical -> hinder base pairing -> mutation) 2 damage sugar (break strand -> repair (non-perfect) -> increased risk of mutation)
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peroxidase group, reaction, members
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hydrogen peroxide -> water + oxygen, 1 catalase (heme w iron) (high substrate specificity) 2 glutathione peroxidase (thiol of GSH as functional group, create GSSG) (low substrate specificity) (Selenium co-factor (as selenocysteine)
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principle of mechanism of small molecule antioxidants
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structure = aromatic + long hydrophilic chain, antioxidant by being formed into a radical and stabilizing it to stop the chain reaction (stabilize due to delocalization of unpaired electron), regeneratable (CoQ = complex III, dismutation, Tocopherol = ascorbic acid)
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reservatrol, belong to which group? source? effect?
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flavonoids/polyphenols (also dark choccolate), red wine, inverse correlation w cardiovascular disease (upregulate Mn-SOD, estrogen-ish effect)
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small molecule antioxidants - which
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1 Coenzyme Q (CoQ)/Ubiquinone (lipophilic) 2 vitamin E/tocopherol (lipophilic) 3 ascorbic acid (hydrophilic)
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sources of NADH?
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1 aerobic glycolysis 2 PDH reaction 3 beta-oxidation 4 citrate cycle 5 ethanol oxidation
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superoxide dismutase, reaction, isoenzymes
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2 superoxides (+2H+) -> (hydrogen)peroxide + oxygen, 2 isoenzymes = Cu/Zn-SOD (u in cytosol), Mn-SOD (mitochondrial)
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4 principle mechanisms for regulation of metabolism
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1 substrate supply 2 allosteric effectors 3 covalent modification of enzymes (kinase/phosphatase, zymogens) 4 induction/repression (transcriptional, induced by substrate, repressed by product)
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co-factor of glucokinase/hexokinase, PFK-1, Phosphoglycerate mutase, Enloase, Pyruvate kinase and isocitrate DH?
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Mg2+
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examples of cross regulation
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1 ↑citrate = inhibit PFK-1 (glycolysis), activate acetyl-CoA carboxylase (FA synthesis) 2 ↑acetyl CoA = inhibit PDH, activate pyruvate carboxylase (gluconeogenesis) 3 ↑malonyl-CoA inhibit CPT-I (beta oxidation)
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glutamine is used for
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1 nucleotide synthesis 2 detoxifivation of amino (-NH2 transport) 3 citrulline synthesis (for urea cycle)
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glycerol phosphate shuttle
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electron-transporter. 1 cytosol: cytosolic glycerol-3P DH use NADH to reduce dihydroxyacetone P to glycerol-3P 2 glycerol-3P diffuse to intermembranous space 3 mitochondrial glycerol-3P DH oxidize to glycerol-3P again, giving the electrons to FADH2 (of complex II) = 1 NADH = 1.5 ATP (6H+ due to bypass of complex I)
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malate/aspartate shuttle
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electron transporter. 1 cytosolic malate DH use NADH to reduce OAA to malate 2 dicarboxylate carrier: malate into mitochondrial matrix, alpha-ketoglutarate out 3 mitochondrial malate DH oxidize it back, releasing NADH 4 aspartate aminotransferase: OAA -> aspartate (glu donate NH2, becomes alpha-ketoglutarate -> dicarboxylate carrier) 5 glutamate\aspartate carrier (asp out, glut in, import 1H+), = 1 NADH -> 9H+ = 2.25 ATP
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metabolic reactions in lysosomes
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hydrolysis of proteins, saccharides, lipids and NAs
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metabolic reactions in peroxisomes
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1 oxidative reactions using oxygen 2 use of hydrogen peroxide 3 degradation of long chain FAs (over 20C)
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net production of ATP molecules from the oxidation of one molecule of glucose, when the glycerol phosphate shuttle is used
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29.5 ATP
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substances that affect complex II of respiratory chain
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1 malonate (similar to succinate, competitive inhibition of succinate DH) 2 thenoyltrifluoroacetona (inhibit electron flow)
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substances that affect complex III of respiratory chain
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1 antimycin A 2 myxothiazol (both inhibit electron transfer to cyt C)
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substances that affect complex IV of respiratory chain
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1 Cyanide 2 Carbon monoxide 3 Azide
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substances that affect transport of electrons from complex I to complex III of respiratory chain
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1 rotenone 2 piericidin 3 amytal
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substances that block the the proton channel/Fo of ATP synthetase
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1 Oligomycin 2 DCCD (dicyclohexylcarbodiimide)
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what happens w AAs during well fed state?
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1 proteosynthesis 2 oxidation (H2O, CO2, urea) 3 transformation to fat in liver 4 enterocytes - Asp, Asn, Glu, Gln -> Ala, Lactate, Citrulline, Pro -> released
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conversion factor for kcal (kilocalorie) to kJ
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1 kcal = 4.2 kJ
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debranching enzyme - components
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1 glycosyltransferase 2 alpha(1->6)glucosidase
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effect of protein phosphatases 1,2
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1 ↓PP-1 inhibitor (by PP2A) 2 ↓phosphorylase kinase (by both) 3 ↑glycogen synthase (PP-1) 4 ↓glycogen phosphorylase 5 ↑FBP-2 (simultaneously inactivate PFK2)
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effects of PKA
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1 ↓glycogen synthase (a->b) 2 ↑glycogen phosphorylase (b->a) 3 ↑protein phosphatase inhibitor-1 4 ↓protein phosphatase-1 (glycogen phosphorylase a->b) (phosphorylate regulatory site 1 and 2) 5 ↑PFK-2 (simultaneosuly inactivate FPB-2) in cardiomyocytes, opposite in liver 6 ↓liver pyruvate kinase 7 ↑hormone-sensitive lipase
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enterocytes, kidney and liver - fate of Gln, Citrulline and Arg?
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1 enterocytes: Gln -> citrulline -> released 2 kidneys: citrulline -> Arg -> released 3 liver: Arg -> urea + ornithine (↑Arg -> ↑urea cycle), ↑Gln -> ↑citrulline -> ↑urea synthesis, ↑citrulline -> ↑urea synthesis
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enzyme that catalyze: 2ADP -> ATP + AMP
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adenylate kinase
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glycogen phosphorylase kinase - what is needed for full activation? effect?
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1 phosphorylation by PKA (2 sites - on alpha and beta subunit) and Ca2+ (delta subunit - has calmodulin w 4Ca2+ sites)(from alpha-adrenergic stimuli in liver or from sarcoplasmic reticulum in muscle), action by gamma subunit ↑phosphorylase (b->a)(w PKA) + ↓glycogen synthase
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GSK-3, full name, what, regulated by?
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Glycogen synthase kinase 3, deactivate glycogen synthase, inactivated by PKB/Akt (from PIP3 from insulin)
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how is glucose transported from blood to enterocytes?
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1 apical membrane: SGLT-1 (also tubule cells of kidney) 2 hexokinase+Glc-6Pase 3 GLUT2
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how is glycogenolysis activated?
|
1 liver: glucaon and adrenaline muscle: adrenaline 2 G protein activate adenylate cyclase: -> cAMP 3 ↑PKA 4 ↑phosphorylase kinase (->phosphorylase (= phosphorylase a) and synthase (to synthase b (inactive)), phosphorylate synthase (= synthase b (inactive))
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|
|
insulin receptor - effect of kinases
|
1 translocation (GLUT-4, insulin R, IGF-IIR) 2 enzyme activity (↑insulin R, ↑protein phosphatases(PP1,2), ↓GSK3, ↑cAMP phosphodiesterase 3B) 3 gene transcription (PEPCK, glucagon, hexokinase II (skeletal m), glucokinase....)
|
|
|
insulin receptor - signaling pathway
|
1 RTK -> ↑IRS 1-4 (insulin receptor substrate) 2 ->↑PI3 kinase (phosphatidyl inositol-3 kinase) (also mSOS which activate MAPK via Ras) 3 -> ↑PDK1\PDPK1 (3-phosphoinositide dependent protein kinase-1) 4 -> ↑PKB\Akt, SGK (Serum and glucocorticoid-inducible kinases), aPKC (atypical PKC), P70S6K (p70 kinase that target S6 ribosomal protein)(also activated by kinase mTOR, from AAs and GFs) -> effect
|
|
|
insulin receptor, type
|
RTK
|
|
|
protein phosphatase-1, structure, regulation, effect
|
bound to regulatory subunit G w 2 phosphorylation sites, active when only site 1 is phosphorylated, inactive when both are, site 1 by insulin (PI-3 kinase), site 2 by PKA phosphorylate (-> protein phosphatase-1 dissociate -> inhibited by protein phosphatase inhibitor-1)(can phosphorylate site 1 and 2), action = ↑glycogen synthase, ↓glycogen phosphorylase kinase
|
|
|
the net production of ATP molecules from the oxidation of one molecule of glucose when the malate/aspartate shuttle is used
|
31 ATP
|
|
|
AMPK (AMP-dependent kinase), from, effect?
|
↑AMP\ATP -> ↑AMPK -> increase cellular energy levels: inhibit anabolic pathways (FA, protein), stimulate catabolic pathways (FA, GLUT4) ("ischemic kinase")
|
|
|
Asp - use
|
1 amino donor in urea synthesis 2 pyrimidine synthesis 3 purine synthesis
|
|
|
desaturatases in humans
|
∆5-, ∆6-, ∆9-fatty acyl CoA desaturase
|
|
|
DHA, full name, formula
|
docosahexaenoic acid (in fish oil), C22:6n-3
|
|
|
drugs inhibiting HMG CoA reductase of cholesterol synthesis?
|
Statins (atorvastatin, lovastatin, mevastatin, pravastatin, simvastatin)
|
|
|
Electron transferrer of reduced flavins from acyl CoA dehydrogenase?
|
Electron-transfer flavoprotein (ETF) -> ETF:ubiquinone oxidoreductase (ETF:QO)
|
|
|
EPA - full name, formula
|
eicosapentaenoic acid (in fish oil), C20:5n-3
|
|
|
extra enzymes of beta-oxidation of unsaturated FAs?
|
1 3,2-enoyl CoA isomerase (cis-∆3 double bond to trans-∆2 double bond) 2 2,4-dienoyl Coa reductase (use NADPH to form trans-∆3 enoyl CoA)
|
|
|
FAD-dependent acyl CoA dehydrogenases
|
1 very-long chain acyl CoA DH(VLCAD) (cant be imported to mitochondria, Long chains (C12-C14 are therefore substrate, and VL are oxidized in peroxisomes) 2 Long chain .. (LCAD)(C8-C20) 3 Medium chain ... (MCAD)(C4-C12) 4 Short chain ... (SCAD, C4-C6)
|
|
|
GLA - full name, formula
|
gamma-linolenic acid (in evening primrose oil), C18:3n-6
|
|
|
Gly - used for
|
1 cellular proteins 2 porphyrin 3 collagen 4 purines 5 creatine 6 glutathione 7 bile salt conjugation
|
|
|
intracellular K+ concentration
|
139 mM
|
|
|
metabolism of adenine
|
1 nuclease: frees nucleotide 2 nucleotidase: adenosine 3 adenosine deaminase: adenosine + H2O -> inosine + NH4+ 4 purine nucleoside phosphorylase: inosine + Pi -> hypoxanthine + Ribose-1P 5 xanthine oxidase: hypoxanthine + H2O + O2 -> xanthine + H2O2 6 xanthine oxidase: xanthine + H2O + O2 -> uric acid + H2O2
|
|
|
metabolism of guanine
|
1 nuclease: free nucleotide 2 nucleotidase: guanosine 3 purine nucleoside phosphorylase: guanosine -> guanine + ribose 1P 4 guanase: guanine -> Xanthine + NH3 5 xanthine oxidase: xanthine + H2O + O2 -> uric acid + H2O2
|
|
|
oxoacyl CoA thiolases/Thiolases
|
1 component of ''trifunctional beta-oxidation enzyme'' (3 last) 2 general thiolase (matrix, broad activity) 3 specific for acetoacetyl CoA
|
|
|
2,3-BPG, found where, effect
|
2,3-BPG shunt in RBCs (from 1,3-BPG to 3P glycerate), ↓affinity of Hb to O2
|
|
|
?
|
1 hyaluronic acid 2 link protein 3 GAG 4 proteoglycan 5 core protein 6 proteoglycan aggregate
|
|
|
cori cycle
|
lactate (from anaerobic glycolysis in muscle) moves to liver, gets converted to glucose, and is released again
|
|
|
GAG
|
repeating dimer of aminosugar and uronic acid
|
|
|
gluconeogenesis, location
|
liver (90%), tubule cells of the kidneys (10%)
|
|
|
Glucose-alanine cycle, purpose
|
remove ammonia from muscle and replenish its energy supply
|
|
|
glucose-alanine, pathway
|
Muscle: glucose -> pyruvate -> alanine (ALT) -> liver -> pyruvate (ALT) -> glucose
|
|
|
insulin effect on GLUT (glucose transport) proteins
|
increase number of GLUT-4 transporters in plasma membrane
|
|
|
main transaminase in muscle
|
alanine transaminase: AA + pyruvate -> alpha-keto acid + Ala
|
|
|
metallothioneines - location and function
|
1 cytosol, of liver, kidney and enterocytes 2 bind, regulate level, transport metals
|
|
|
name of proteins whose SH group bind metal ions (w 2+) such as Cu2+, Zn2+, Hg2+, Cd2+
|
metallothioneines (rich in cysteine)
|
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|
proteoglycan
|
core protein + GAG
|
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|
transport of NH3 to liver and kidney, by which AA, via which enzyme
|
Gln, Gln synthetase
|
|
|
transport of reducing equivalents to mitochondria, mechanisms
|
malate-aspartate shuttle, glycerol phosphate shuttle
|
|
|
why is ammonia toxic?
|
interact w alpha-ketoglutarate and make it limiting for krebs cycle
|
|
|
Coenzyme
|
Organic molecule slightly bound to the apoenzyme - undergo a chemical change and are released (NAD, FAD, CoQ)
|
|
|
Cofactor
|
A nonprotein component essential for the normal catalytic activity of an enzyme - can be organic molecules = coenzymes/prosthetic group or inorganic ions (apoenzyme + cofactor = functioning holoenzyme)
|
|
|
intracellular bicarbonate concentration
|
12 mM
|
|
|
Intracellular Cl- concentration
|
4 mM
|
|
|
Intracellular Na+ concentration
|
12 mM
|
|
|
intracellular pH value
|
a 7.2
|
|
|
Isoenzyme
|
Enzymes that have the same catalytic activity, but different primary structure
|
|
|
Myelin sheath - composition of fat and protein
|
80% lipid (sphingomyelin and galactocerebroside) and 20% protein (myelin basic protein (MBP), myelin oligodendrocyte glycoprotein (MOG))
|
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|
Myosin light chain (MLC) and MLCK
|
MLC is small regulatory subunits found on myosin heads of smooth muscle, MLCK cause crossbridge formation between myosin heads and actin
|
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|
Prosthetic group
|
Organic molecule tightly bound to the apoenzyme and remain associated w the enzyme during the reaction (Heme, biotin)
|
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|
Purine nucleotide cycle - 1-5?
|
1 Myoadenylate deaminase (AMP deaminase isoenzyme)(mutation = excessive fatigue following excercise) 2 adenylosuccinate synthetase 3 adenylosuccinate lyase 4 Asp 5 Fumarate (TCA anaplerotic for muscle)
|
|
|
Purine nucleotide cycle - function
|
anaplerotic of fumarate (+OAA) for TCA cycle in skeletal muscle,
|
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|
Skeletal muscle - mechanism of contraction after release of Ca2+
|
1 Ca2+ bind to troponin C (troponin = C(Ca2+),T(Tropomyosin)) of actin 2 troponin allosterically alter tropomyosin, troponin T allows tropomyosin = unblock myosin actin binding site 3 Rigor configuration (= rigor mortis)(myosin WO nucleotide is tightly bound to actin) 4 ATP bind to myosin -> reduce its affinity to actin (release) and allows it to move along the filament 5 hydrolysis = ADP and P remain tightly bound 6 Release of Pi -> power stroke (move back to its rigor original conformation)
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|
Skeletal muscle - stimuli for contraction?
|
1 Ach trigger action potential in muscle 2 Spread through T tubules 3 cause relase of Ca2+ from terminal cisternae of SR (1st dihydropyridine receptors in membrane cause opening of ryanodine receptors in SR)
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|
Skeletal muscle - termination of contraction
|
Ca2+ is removed by active transport into the SR after the action potential ends
|
|
|
Smooth muscle contraction - mechanism (1-5)?
|
1 Ca2+ 2 Calmodulin 3 Ca2+-Calmodulin complex 4 MLC 5 MLCK
|
|
|
1st reaction of purine synthesis
|
Glutamine-PRPP amidotransferase: PRPP + Glu + H2O
|
|
|
1st step of cholesterol synthesis - reaction and enzyme
|
HMG CoA synthase: acetoacetyl CoA + acetyl CoA -> HMG (acetoacetyl thiolase produce acetoacetyl CoA)
|
|
|
androstenedione to testosterone (C19), reaction, where
|
hydrogenation of DHEA at 17 in leydig cells (dihydrotestosterone is formed by reduction)
|
|
|
DHEA to androstenedione
|
isomerization reaction
|
|
|
final step of GMP synthesis
|
GMP synthetase: XMP (xanthosine) + ATP + Gln -> GMP + ADP + Glu
|
|
|
how is estradiol formed?
|
Testosterone (C19) -> Estradiol (C18): removal of C18, aromatization (aromatase in ovaries, adipose) of A ring
|
|
|
How is pregnenolone produced from cholesterol?
|
6C atoms from the side chain is removed (= 21C)
|
|
|
Main difference between purine and pyrimidine synthesis
|
purine = base is built on ribose, pyrimidine = base is built first, then attached to ribose
|
|
|
Nucleotide salvage pathway - what
|
synthesis of nucleotides from bases or nucleosides, inhibit de novo synthesis
|
|
|
PAPS - full name, what? created from?
|
3'-phosphoadenosine-5'-phosphosulfate (PAPS), used as sulfate donor, from 2ATP and S04
|
|
|
Pregnenolone (21C) to aldosterone (21C), chemical changes
|
1 transformed to progesterone (isomerase) 2 transformed to aldosterone (hydroxylated at 11 and 21) (in zona glomerulosa)
|
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Pregnenolone (21C) to cortisol - chemical changes
|
1 transformed to progesterone (isomerase) 2 transformed to cortisol (hydroxylated at 11,17,21) (in zona fasciculata)
|
|
|
Pregnenolone (21C) to DHEA (dehydroepiandrostenedione) (C19), chemical changes
|
2C side chain cleavage, hydroxylation at 17 (in zona reticularis of adrenal cortex)
|
|
|
PRPP (phosphoribosyl-1PP), created by? regulation?
|
PRPP synthetase: ATP + Ribose-5P/Phosphoribose -> PRPP + AMP, regulated by feedback inhibition of nucleoside di- and triphosphates
|
|
|
substrate common for both pyrimidines and purines?
|
PRPP
|
|
|
Dihydrofolate reductase can be inhibited by the exogenous agent
|
Methotrexate
|
|
|
Final step of AMP synthesis
|
Adenylosuccinase: Adenylosuccinate -> AMP + Fumarate
|
|
|
final step of CTP synthesis
|
CTP synthetase: UTP + ATP + Gln + H2O -> CTP + Glu + ADP + Pi
|
|
|
Final step of TMP synthesis
|
Thymidylate synthase: dUMP + methyleneTHF -> TMP + DHF
|
|
|
Final step of UMP synthesis
|
OMP decarboxylase: OMP -> UMP + CO2
|
|
|
Folate to co-factor tetrahydrofolate (THF)?
|
Dihydrofolate reductase, 2 steps, use NADPH
|
|
|
form of THF in nucleotide synthesis, co-factor in transferase
|
methylene-THF, B6/PLP
|
|
|
function of methyl-THF, cofactor
|
transfer methyl group to homocysteine to make it into met, b12 as cofactor, (met -> homocysteine via SAM)
|
|
|
IMP - full name, base, common precursor to
|
Inosine monophoshate, hypoxanthine, AMP and GMP
|
|
|
important intermediates of purine synthesis
|
1 5'-Phosphoribosylamine (precursor to IMP) 2 IMP (inosine MP)
|
|
|
Principle donor of methylene group to THF
|
Serine (by glycine hydroxymethyltransferase - becomes glycine)
|
|
|
Regulation of nucleotide synthesis
|
1 PRPP synthetase (purine and pyrimidine nucleoside di- and triphosphates) 2 nucleotide synthesis = feedback inhibition 3 nucleoside diphosphate reductase (+nucleoside triphosphates, - dATP)
|
|
|
regulation of pyrimidine synthesis, feed-forward activation? feed-back inhibition?
|
feed-back inhibition: and UTP CP synthetase II, UMP on OMP decarboxylase, feed-forward activation: ATP on CPSII and orotate phosphoribosyl transferase
|
|
|
Substrates for pyrimidine synthesis
|
1 Carbamoyl P (Gln, CO2, 2ATP) 2 Asp 3 PRPP 4 Methylene-THF (only for thymidine)
|
|
|
synthesis of 2-deoxyribonucleotides
|
ribonucleotide reductase, become free radical to steal H (rare mechanism)(electrons from thioredoxin (regenerated from NADPH))
|
|
|
THF can carry
|
Methyl, Formyl, Methylene....
|
|
|
AAs w positive side chains
|
HAL. Histidine, Arginine, Lysine
|
|
|
Allopurinol
|
competitive inhibitor of xanthine oxidase (hypoxanthine -> uric acid), used for hyperuricemia/gout
|
|
|
Biochemical standard chemical conditions for Gibbs energy - pressure, pH, temperature, molar
|
pH = 7 (chemical conditions = 0), 1ATM, 25C, 1M
|
|
|
Conditionally essential AAs
|
Histidine, Arginine
|
|
|
Cystine structure
|
CySteine contains C-S (Sulphur attached to Carbon)
|
|
|
definition of Gibbs energy
|
1 Change in Gibbs energy is equal to the maximum amount of work that can be done by the reaction (reaction spontaneous? will it occur?) 2 Change in Gibbs energy is a measure of displacement from equilibrium (∆G = 0 = equilibrium)
|
|
|
difference between purine and pyrimidine metabolism
|
1 formation of N-glycosidic bond: purines = 1st step, pyrimidine = ring formed first 2 location: purine = cytoplasm, pyrimidine = cytoplasm + CPSII in mitochondria 3 degraded products
|
|
|
Enthalpy (H)
|
energy released or consumed during a reaction, -/< 0 = release energy/exergonic
|
|
|
Formula of Gibbs free energy: 1 normal 2 related to K
|
1 ∆G = ∆H - T∆S 2 ∆G = ∆Go + RT ln (equlibrium constant - products on top)
|
|
|
Gibbs energy - when will a reaction occur? when is it at equilibrium? When will it not occur?
|
1 ∆G= < 0 2 ∆G=0 3 ∆G= > 0
|
|
|
Michaelis-Menten curve, what is competitive inhibiton and what is noncompetitive?
|
1 competitive inhibition 2 Noncompetitive inhibition
|
|
|
Stages of meiosis
|
IPMAT. Interphase, Prophase, Metaphase, Anaphase, Telophase
|
|
|
The 10 essential AAs
|
I saw, he phoned at 3:09 and met licentious (frekk/uanstendig) Argentines - Lucy, Tracey and Val. I saw (Isoleucine) He (Histidine) Phoned at (Phenylalanine) 3:09 (Threonine) Met (Methionine) Licentious (Lysine) Argentines (Arginine) Lucy (Leucine) Tracey and (Tryptophan) Val (Valine) / PVT.(= private in military lingo) TIM HALL: Phe, Val, Thr, Trp, Ile, Met, His, Arg, leu, Lys
|
|
|
The four fates of pyruvate
|
GALA. G(Glucose)A(Alanine)L(Lactate)A(Acetyl Co-A)
|
|
|
Valine structure
|
V-shaped group (just stick a V up your R!)
|
|
|
2nd law of thermodynamics
|
All closed becomes increasingly disordered
|
|
|
Arginine - structure
|
Argentina PRayiN' for CNN (R = Pr(propyl)-N-CNN(Carbon, Nitrogen, Nitrogen)
|
|
|
Entropy (S)
|
disorder of system
|
|
|
Leucine - structure
|
Like the greek letter lambda λ (V with C above as R group)
|
|
|
Lineweaver Burk plot - what is competitive inhibition and what is noncompetitive?
|
1 Noncompetitive inhibition 2 Competitive inhibiton
|
|
|
Lineweaver-Burke plot - difference between graphs of competitive and non-competitive inhibition
|
Two crossed swords - in competition. In non-competitive inhibition - they do not cross
|
|
|
Location of catecholamine degrading enzymes
|
Cytoplasm: COMT(catechol-O-methyltransferase), Mitochondria: MAO A/B
|
|
|
Methionine - structure
|
C(S)ee CoxSaSkie v (-C-C-S-C)
|
|
|
Ortho-, meta- and para- substititons of aromatic rings
|
Or-two met-a-tree para-four. Or-two (Ortho-2) Met-a-tree (Meta-3) Para-four (Para-4, parallel to C1)
|
|
|
Proline - structure
|
R is shaped like a PentagoN with Nitrogen in one corner
|
|
|
Redox reactions - what happends to electons
|
OIL RIG. Oxidation Is Loss, Reduction Is Gain
|
|
|
Serine - structure
|
Think of a searin` (brennende) pain caused by drinking methanol (R = CH2OH/methanol)
|
|
|
Synthesis of catecholamines, enzymes
|
Tired Dopes Dominate Norway. Tired (Tyrosine) Dopes (DOPA/Dihydroxyl-L-phenylalanine) Dominate (Dopamine) Norway (Noradrenaline). Hide de ho: HiDe (hydroxylase), de (decarboxylase), HO (beta-OH-lase/hydroxylase)
|
|
|
Threonine - structure
|
Threonine has 3 oxygen atoms (three-O) and nine H atoms (-nine) (R = Ethanol)
|
|
|
Urea cycle - mnemonic
|
Ordinarily careless crappers are also frivolous (lettsindige) about urination. Ordinarily (Ornithine) Careless (Carbamoyl-phosphate) Crappers (Citrulline) Are (Aspartate) Also (Arginosuccinate) Frivolous (Fumarate) About (Arginine) Urination (Urea)
|
|
|
Which nucleotides are purines, and what are they`re shape?
|
All girls are pure and wear bras. All (Adenine) Girls are (Guanine) Pure (Purine) and wear bras (bras are two-ringed structures - so are purines!)
|
|
|
Adrenaline mechanism
|
ABC of adrenaline. Adrenaline -> activates beta receptors -> increases cAMP
|
|
|
B vitamin names
|
The Rhythm Nearly Proved Contagious (in increasing order). Thiamine (B1), Riboflavin (B2), Niacin (B3), Pyridoxine (B6), Cobalamin (B12)
|
|
|
Carbon monoxide - electron transport chain target
|
CO blocks CO. Carbon monoxide/CO blocks cytochrome oxidase (CO)/complex IV
|
|
|
Chemical processes going on in both cytoplasm and mitochondria
|
Use both arms to HUG. These reactions occur in both cytoplasm and mitochondria. Heme synthesis, Urea cycle, Gluconeogenesis
|
|
|
Dicarboxylic acids - C2-C8
|
Oh, My, Such Good Apple Pie. Oxalic, Malonic, Succinic, Glutaric, Adipic, Pimelic
|
|
|
Electron transport chain - rotenone's (inceticide, vs scabies) site of action
|
Rotenone is a site specific inhibitor for complex one
|
|
|
Glycolysis steps
|
Goodness Gracious, Father Franklin Did Go By Picking Pumpkins (to) Prepare Pies. Glucose, Glucose-6-P, Fructose-6-P, Fructose-1-6diP, Dihydroxyacetone-P, Glyceraldehyde-P, 1,3-Biphosphoglercerate, 3-Phosphoglycerate, 2-Phosphoglycerate (to), Phosphoenolpyruvate/PEP, Pyruvate ('Did', 'By', and 'Pies' tell you the first part of those three: di-, bi-, py-.
|
|
|
How to differentiate structure of glucsose and fructose
|
Fructose: five-ring, Glucose: hexaGon
|
|
|
Increased anion-gap acidosis
|
MUDPIES: Methanol, Uremia, Diabetes, Paraldehyde, Idiopathic (lactic acidosis), Ethylene glycol, Salicylates
|
|
|
Indirect reacting bilirubin - unconjugated or conjugated bilirubin?
|
Indirect-reacting bilirubin = Unconjugated bilirubin (both start with vowels)
|
|
|
Insulin - what to be imported into cells?
|
Insulin stimulates 2 things to go. Potassium, Glucose
|
|
|
Normal anion gap acidosis
|
RAGE: R(renal tubular acidosis, respiratory acidosis) A(acetazolamide, ammonium chloride) G (GI: diarrhea, enteroenteric fistula, ureterosigmoidostomy) E (endocrine: Addisons, spironolactone, triamterene, amiloride, primary hyperparathyroidism)
|
|
|
Phosphorylation cascade - action during low glucose
|
In the phasted (fasted) state - phosphorylate! (The phosphorylation cascade becomes active when blood glucose levels is low)
|
|
|
Some drugs w zero-order kinetics
|
Constantly aspiring to phone ethan. Constantly (zero-order kinetics) aspiring (aspirin) to phone (phenytoin) ethan (ethanol)
|
|
|
TCA cycle intermediates mnemonic
|
A certificate in karma sutra should further my orgasm: Acetyl-CoA, Citrate, Isocitrate, Alpha-ketoglutarate, Succinyl-CoA, Succinate, Fumarate, Malate, Oxaloacetate
|
|
|
Adrenal cortex layers and products
|
Go find Rex, make good sex. Layers(outer->inner): Glomerulosa, Fasciculate, Reticulata. Respective products: Mineralocorticoids, Glucocorticoids, Sex hormones
|
|
|
Coagulation common pathway - factors in order
|
10 + 5 - 2 = 13 (factor X -> factor V -> factor II -> factor XIII)
|
|
|
Enzyme kinetics - competitive vs non-competitive inhibition
|
With kompetitive inhibiton: Km increase, no change in Vmax. With Non-kompetitive inhibition: No change in Km, Vmax decrease
|
|
|
Enzymes - classification
|
Over The HILL: Oxidoreductases, Transferases, Hydrolases, Isomerases, Ligases, Lyases (enzymes get reactions over the hill)
|
|
|
G6PD: oxidant drugs inducing hemolytic anemia
|
AAA. Antibiotic (ie sulfamethoxazole), Antimalarial (ie primaquine), Antipyretics (acetanilid)
|
|
|
Gibbs free energy formula
|
Good Honey Tastes Sweet. (delta)G = H - T(delta)S
|
|
|
Glucagon mechanism
|
Mr. Gluca has Gone to the cAMP to bring out some Glucose. Glucagon elevates glucose by cAMP
|
|
|
Glycolysis enzymes
|
High Profile People Act Too Glamorous, Picture Posing Every Place. Hexokinase, Phosphoglucose isomerase, Phosphofructokinase (PFK), Aldolase A, Triose phosphate isomerase, Glyceraldehyde-3-phosphate dehydrogenase, Phosphoglycerate mutase, Enolase, Pyruvate kinase
|
|
|
Golgi complex - functions
|
Golgi Distributes A SPAM. Distributes proteins and lipids from ER, Add mannose onto specific lysosome proteins, Sulfation of sugars and selected tyrosine, Proteoglycan assembly, Add O-oligosugars to serine and threonine, Modify N-oligosugars on asparagine
|
|
|
Heme synthesis - amino acid precursors to basic units of porphyrins, heme (pyrrole ring)
|
Dracula wants Suck a Co-ed's blood (think heme) with his Glystening teeth! Succinyl-CoA and Glycine
|
|
|
Malate-aspartate shuttle
|
MAD commute. Malate in, Alpha-ketoglutarate and D (Aspartate) out
|
|
|
Phenylketonuria - which enzyme is deficient
|
PHenylketonuria is caused by a deficency of: Phenylalanine Hydroxylase
|
|
|
Sickle cell disease pathophysiology
|
SICKle cell disease is due to a Substition of the SICKsth amino acid of the B chain
|
|
|
Vitamin B3/Niacin/Nicotinic acid deficiency = pellegra - symptoms
|
The 3 Ds (note vitamin B3): Dermatitis, Dementia, Diarrhea
|
|
|
Vitamin K-dependent clotting factors
|
Several Tend To Nicely Stop Clots. Factor Seven, Ten, Two, Nine, Protein S, Protein C
|
|
|
A - base, nucleoside
|
adenosine, adenine
|
|
|
C, base, nucleoside
|
cytosine, cytidine
|
|
|
debranching enzyme
|
amylo-alpha1 → 6-glucosidase
|
|
|
G - base, nucleoside
|
guanine, guanosine
|
|
|
glycogen branching enzyme
|
amylo-(1,4-1,6)-transglycosylase
|
|
|
glycogenesis in liver, regulation
|
+ Glc, - Glucagon
|
|
|
glycogenesis in muscle, regulation
|
+ insulin, - epinephrine
|
|
|
glycogenesis, regulatory step
|
by glycogen synthase (phosphorylated\b = inactive)
|
|
|
glycogenesis, step 1-2
|
1 Glc -> Glc-6-P in hepatocytes by glucokinase, 2 Glc-6-P -> Glc-1P (phosphoglucomutase)
|
|
|
glycogenesis, step 3-4
|
3 Glc-1P + UTP -> UDP-Glucose (Glc-1P uridylyltransferase) 4 UDP-Glc to glycogen (glycogen synthase, only 1-4)
|
|
|
Glycogenesis, step 5-6
|
5 6-7 Glc residues is removed and branched on (branching enzyme) 6 elongation by glycogen synthase
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glycogenolysis, step 1-2
|
1 phosphorolysis of 1-4 -> Glc-1P (glycogen phosphorylase) and debranching enzyme2 Glc-1P -> Glc-6P (phosphoglucomutase)
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glycogenolysis, step 3
|
only liver+kidney+enterocyte. 3 Glc-6P -> Glc (Glc-6P phosphatase)
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T - base, nucleoside
|
thymine, thymidine
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U - base, nucleoside
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uracil, uradine
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creatinine
|
endproduct of creatine phosphate in muscles, excreted in urine
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glutathion
|
peptide which as antioxidant properties
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Glycogenolysis, +
|
Epinephrine+glucagon (via phosphorylase kinase), AMP, Ca2+ (muscle)
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glycogenolysis, -
|
insulin (via phosphorylase kinase), ATP, Glc-6P, Glc
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oxidative phase of pentose cycle, regulation
|
Glc-6P to ribulose 5P+CO2+2NADPH, Glc 6P DH (by NADPH\NADP+ ratio)
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pentose cycle, location
|
all tissue in cytoplasm, pri RBC, liver, mammary gland, testis, adrenal cortex
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pentose cycle, purpose
|
create NADPH+H+, ribose-5-phosphate
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pentose cycle, regenerative phase
|
produce ribose 5P, glyceraldehyde 3P, Fruc 6P
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pentose cycle, substrate
|
Glc-6-P
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Pentose cycle, synonym
|
hexose monophosphate pathway (HMPP)
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PFK-2, location
|
part of bifunctional enzyme (w FBP-2), pri liver
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PFK-2, product
|
Fru-2,6-BP, activate PFK-1 and inhibit Fru-1,6-BPase
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PFK-2, regulation
|
phosphorylated = active PFK-2 by (high insulin/glucagon)
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regulatory step of glycogenolysis, active form, regulatory enzyme
|
glycogen phosphorylase, phosphorylated\a = active, phosphorylase kinase
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through inner membrane of mitochondria can go (whole molecule)
|
citrate
|
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|
?
|
1 hyperthyroidism 2 DM 3 normal 4 impaired glucose tolerance 5 myxedema (form of hypothyroidism w hard edema due to mucus = myx)
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cortisol (main glucocorticoid), effect
|
1 ↑proteolysis (↑gluconeogenesis = ↑glycemia) 2 antinflammatory (reduce histamine release and stabilize lysosomal membranes) 3 ↑BP (↑sensitivity of vasculature to catecholamines)
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cortisol, stimuli for release
|
''stress hormone'', hypothalamus secrete CRH (corticotropin-releasing hormone) = pituitary ssecrete ACTH (adrenal corticotropic hormone) = ↑cortisol
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glucagon, effect
|
glycogenolysis (hepatic phosphorylase) &gluconeogenesis + release of glucose from liver (also decrease gastric motility+gastric secretion+pancreatic secretion and increase urinary excretion of N and K)
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glucagon, produced by
|
alpha cells of islets of Langerhans
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glucagon, stimuli for release
|
1 hypoglycemia 2 ↑catecholamines 3 ↑plasma AAs (to protect from hypoglycemia if an all-protein meal is consumed) 4 sympathetic NS 5 CKK
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GLUT-4
|
skeletal muscle, heart muscle, adipose tissue
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glycemia-related action of catecholamines
|
1 ↑insulin secretion 2 ↑glucagon secretion 3 ↑ACTH secretion 4 ↑lipolysis in adipocytes
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insulin, effects
|
1 ↑GLUT-4 2 ↑glycolysis 3 ↑glycogenesis 4 ↑FA synthesis (force adipocytes to take in blood lipids and convert them to TGs) 5 ↑protein synthesis (by increased cellular AA uptake)
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isomaltose
|
two glucose molecules are attached by an alpha1-6 link, from digestion of branching part of amylopectin
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lactulose
|
galactose + fructose (synthetic laxative, colonic acidifer = remove ammonia from blood w liver failure)
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Lineweaver-Burke curve, what, detect what
|
michaelis-menten plot w double reciprocal values (x = 1/s, y = 1/v), 1/vmax = crossing point of y, 1/km = crossing point of x
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Michaelis-Menton curve, x and y? detect what?
|
x = substrate concentration, y = velocity of reaction, Vmax and Km (Michaelis Menten constant, vmax/2)
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oGTT, dm2 if
|
1 morning glycemia higher than 8 2 higher than 11.1 after 2h
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oGTT, full name, what
|
oral glucose tolerance test, 1 fast overnight 2 measure glucose 3 give glucose (75g) 4 measure after (30, 60, 90, 120min)
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postprandial glycemia
|
s-glucose test after meal
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alkaline phosphatase (ALP), what
|
group name of relatively non-specific hydrolytic enzymes that cleave many phosphoric monoesters ( R-O-PO32- + acceptor -> R-OH + acceptor-PO32-)
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ALP, function
|
1 involved in transport processes in the liver 2 participate in bone precipitation by osteoblasts (found on membrane) 3 involved in Ca2+ absorption in intestine
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ALP, linked pathologies
|
hepatic isoform (biliary obstruction, hepatitis, alcohol-induced liver disease, cirrhosis, hepatoma, mononucleosis), bone isoform (hyperparathyroidism, bone fractures, bone tumors (osteosarcoma))
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ALP, pH optimum, functioning at
|
10.5, above 7
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ALP, serum value above 15y
|
0.66-2.20 mkat/L
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ALP, which isoforms are measured diagnostically?
|
Bone and liver
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amino acids, pK1 (-COOH) & pK2 (-NH3+) (ca)
|
2 & 9-10
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anion gap, normal value
|
16-20
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base excess
|
the amount of strong acid that would have to be added /volume of blood to titrate it to 7.4 when pCO2 is 40mmHg
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glucose determination by photometer
|
enzymatic + photometry, 1 glucose oxidase (h2o2+gluconate) 2 peroxidase (phenol+ 4-aminoantipyrine) 3 scarlet color (498 nm)
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glucotouch
|
enzymatic+photometry, 1 glucose oxidase (give h2o2+gluconate) 2 peroxidase (give product w blue color)
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hyperparathyroidism
|
increased PTH = increased Ca2+, decreased Pi
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isoenzymes and isoforms of ALP
|
isoenzymes = placental, intestinal, tissue nonspecific (bone, liver, kidney)
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Lambert Beer's law
|
f (conversion factor) = cST/AST
|
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|
main AA residues working as buffers, and their r pK
|
asp - 3.9, glu - 4.1, his 6
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oGTT, parts of the curve, dependent on what
|
1 ascending (rate of resorption from intestine) 2 peak level (liver function (glycogenesis+insulin action in the liver) 3 descending part (insulin action, characteristic of DM)
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transporters in ascending loop of henle
|
Na+K+2Cl- transporter
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why can't glutamine's R group work as a buffer
|
contains amide group
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catecholamines and glucagon, most effective on which hyperglycemic reaction?
|
glycogenolysis
|
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ethanol degrading enzymes
|
1 alcohol DH (cytoplasm), acetaldehyde DH (mitochondria) (prim responce, inefficient, use (and deplete) NAD+)) 2 microsomal (from centrifugation of ER) ethanol oxidation system (MEOS)/CYP450 2E1 (only replace ethanol DH which is the rate-limiter, use (and deplete) NADPH)
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functional unit of liver
|
hepatic acinus
|
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hepatic encephalopathy - cause
|
accumulation of ammonia due to liver insufficiency (ammonia from AA metabolism and from intestinal bacteria)
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hormones involved in fasting state
|
1 glucagon 2 catecholamines 3 glucocorticoids
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how can acetate go into metabolism?
|
acetate-CoA ligase (need ATP) activate acetate to CoA
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N-acetylneuraminic acid (NeuAc, NANA)
|
most common form of sialic acids in mammals
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pentose cycle is important for
|
FA synthesis (NADPH), antioxidant systems (NADPH)
|
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perivenous hepatocytes, where, specialized function
|
in zone III of hepatic acinus (next to central vein), low O2 = glutamate synthesis from ammonia, biotransformation of xenobiotics (SER), reductive reactions (lipid synthesis, ketogenesis, glygoenesis)
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sialic acids (Sia), what, where
|
N- and O- acyl derivates of neuraminic acid, constituents of gangliosides and of many glycoproteins and mucoproteins
|
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|
total oxygen consumption of the liver?
|
20-30%
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vitamins metabolized in the liver?
|
1 Vit A/retinoic acid, produced from provitamin (beta caroten) in the liver, stored 2 vit D - 1st hydroxylation
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where is periarterial hepatocytes found, and what is their specialized function?
|
in zone I of liver acinus (next to portal triad), high O2 allow urea synthesis (ATP-demanding) and other oxidative reactions (TCC, rspiratory chain, beta oxidation, gluconeogenesis, proteosynthesis, cholesterol synthesis)
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which tissue can we find glucokinase in?
|
beta cells and liver
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Whichs FFAs can be directly absorbed in the blood?
|
FFAs shorter than 12 C's
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Why can't glucose from glycogenolysis from muscle cells be exported?
|
lack glucose-6 phosphatase
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|
after how many hours of starvation is the contribution of glycogenolysis and gluconeogenesis equal?
|
a 16h
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|
bile acid, structure
|
steroids w 24 carbons
|
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|
carnityl acyltransferase I (transfer FAs into mitochondria), regulation
|
- malonyl-CoA, increased ratio of insulin/glucagon
|
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effects of alcohol on metabolism
|
oxidation produce 2 NADH (ethanol DH, acetaldehyde DH), disposal of these cause 1 ↑pyruvate -> lactate (= lactic acidosis (=gout by inability to excrete uric acid), hypoglycemia) 2 lipid synthesis (by hindering beta oxidation)(= more TG = fatty liver, hyperlipidemia = infarcts, ketogenesis)
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|
|
glucocorticoids, most effective on which hyperglycemic reaction?
|
gluconeogenesis
|
|
|
how is acetone formed in ketogenesis?
|
by non-enzymatic decarboxylation from acetoacetate
|
|
|
how is beta-hydroxybutyrate formed in ketogenesis?
|
acetoacetate by beta-hydroxybutyrate DH
|
|
|
how many ATP is needed to produce 1 urea?
|
3 ATP (2 for carbamoyl phosphate synthetase I(CPSI)), 1 for argininosuccinate synthetase)
|
|
|
how many ATP is used to create 1 glucose from 2 pyruvate?
|
6 ATP
|
|
|
secondary bile acids
|
synthesized in the intestine by dehydroxylation of primary bile acids at C7
|
|
|
spectrin
|
large cytoskeletal protein found on the inner cell membrane of rbcs associated w actin, mutation = ellipto/spherocytosis
|
|
|
tumor necrosis factor - role in metabolism during stress response
|
adipose tissue = + TG to FAs, - VLDL deposition
|
|
|
what is added to bile acids to form bile salts?
|
glycine and taurine
|
|
|
which hormones does the liver produce?
|
somatomedines (IGF-I and II)
|
|
|
B-vitamins
|
1 Vitamin B1/Thiamine 2 Vitamin B2/Riboflavin 3 Vitamin B3/Niacin 4 Vitamin B5/Pantothenic acid 5 Vitamin B6/Pyridoxine 6 Vitamin B7/Vitamin H/Biotin 7 Vitamin B9/Folic acid 8 Vitamin B12/Cobalamins
|
|
|
beta-carotene, provitamin for? structure? toxic?
|
vitamin A/retinol, 2 x retinol, non-toxic
|
|
|
causes of hepatocellular hyperbilirubinemia
|
1 decreased uptake of bilirubin by hepatocytes 2 deficit in conjugation 3 defect of active transport of bile
|
|
|
how are vitamins classified?
|
on account of their biological and chemical activity - not their structure, means that 1 vitamin = a number of vitamer compounds that all show the same/similar biological activity
|
|
|
metabolism of vitamins in the liver
|
1 Provitamins -> vitamins (carotenes -> vit A, 25-hydroxylation of vit D, cleave side chain of vit K) 2 storage (vit b12) 3 synthesize nicotinic acid from Trp 4 b vitamins -> coenzymes
|
|
|
neonatal jaundice, cause
|
increased hemolysis, decreased activity of glucuronosyltransferase
|
|
|
phase I of starvation, duration, source of glucose
|
4h, exogenous
|
|
|
phase II of starvation, duration, source of glucose
|
4-16h, 1 glycogenolysis 2 gluconeogenesis (muscle and adipose tissue use glucose at diminished rate)
|
|
|
phase III of starvation, duration, source of glucose
|
16h-1.5d, 1 gluconeogenesis 2 glycogenolysis (brain still use glucose)
|
|
|
phase IV of starvation, duration, source of glucose, tissues using glucose
|
1.5d-24d, gluconeogenesis (also renal), brain (start using KBs), renal medulla, rbcs, (muscle)
|
|
|
phase V of starvation, duration, source of glucose, tissues using glucose
|
24d->, gluconeogenesis (hepatic and renal), brain (most by KBs), rbcs, renal medulla
|
|
|
retinol and retinoic acid - relation
|
retinol is oxidized to retinoic acid in 2 steps (retinol - retinal - retinoic acid), process cannot be reversed
|
|
|
Vitamin A/retinol - function
|
1 prosthetic group to rhodopsin in retina (11-cis/trans retinal) 2 morphogen via Hox genes (RAREs - retinoic acid response elements and RAR - retinoic acid receptor)) (teratogen in high doses) 3 contribute to thyroxine formation
|
|
|
Vitamin D/Cholecalciferol - deficiency disorders
|
1 Rickets (children, easy breakable bones and deformation(bow legged)) 2 Osteomalacia (adults, easy breakable bones, elderly (malnutrition, no sun))
|
|
|
vitamins
|
group of organic substances (water/fat soluble), present in minute amounts in natural food - most can't be produced endogenously, essential to normal metabolism, most are co-enzymes
|
|
|
action of PDH kinase
|
inhibit E1
|
|
|
action of PDH phosphatase
|
activate E1
|
|
|
anaerobic metabolism predominate in
|
cornea+lens, kidney medulla, testes, WBCs, RBCs
|
|
|
arsenic poisoning
|
inhibit enzymes w lipoic acid, antagonist to Pi as substrate for glyceraldehyde 3P dehydrogenase
|
|
|
E1\pyruvate decarboxylase, cofactors
|
NADH, TPP
|
|
|
E2\dihydrolipoyl transacetylase, cofactor
|
lipoic acid, CoA
|
|
|
E3\dihydrolipoyl dehydrogenase, cofactor
|
FAD, NAD+
|
|
|
effect of glucagon on glucokinase, PFK-1 and pyruvate kinase in the liver
|
inhibit
|
|
|
effect of insulin on glucokinase, PFK and pyruvate kinase in liver
|
+
|
|
|
enzyme forming lactate, cofactor
|
lactate dehydrogenase, NADH
|
|
|
enzymes of pyruvate dehydrogenase complex
|
E1\pyruvate decarboxylase, E2\dihydrolipoyl transacetylase, E3\Dihydrolipoyl dehydrogenase
|
|
|
fructose 2,6-BP
|
by PFK-2 (kinase+phosphatase, kinase is active when dephosphorylated by protein kinase A (via insulin))
|
|
|
function of glucokinase
|
pancreas = glucose sensor, liver = facilitate glucose phosphorylation during hyperglycemia
|
|
|
glucokinase, +
|
glucose (frees glucokinase from regulatory protein in nucleus)
|
|
|
glucokinase, -
|
fructose-6P (promote regulatory protein (GKRG) to bind glucokinase in nucleus)
|
|
|
glucokinase, properties
|
high Km, high Wmax
|
|
|
glucose enter cell by
|
Na+-independent facilitated diffusion, Na+-monosaccharide cotransporter system
|
|
|
GLUT1
|
abundant in RBC and brian
|
|
|
GLUT2
|
liver+kidney+pancreas, bilateral transport
|
|
|
GLUT3
|
primary for neurons
|
|
|
GLUT4
|
high in adipose and muscle, activated by insulin
|
|
|
GLUT5
|
small intestine+testes, primarily for fructose
|
|
|
GLUT7
|
liver+gluconeogenic tissue, mediate across ER membrane
|
|
|
glycolysis, location
|
cytoplasm
|
|
|
hexokinase, -
|
glucose-6P
|
|
|
how does insulin regulate glucokinase, PFK1 and pyruvate kinase
|
stimulate
|
|
|
lactate can be...
|
used by the liver to make glucose
|
|
|
most common cause of congenital lactic acidosis
|
deficiency of E1 of pyruvate dehydrogenase complex
|
|
|
most frequent electron donor in anabolic reactions
|
NADPH
|
|
|
most frequent electron donor in catabolic reactions
|
NAD
|
|
|
most important control point and rate-limiting step of glycolysis
|
PFK-1
|
|
|
Na+-independent monosaccharide facilitated diffusion transport
|
GLUT1-GLUT14
|
|
|
Na+-monosaccharide cotransport system, carrier?
|
sodium-dependent-glucose transporter (SGLT)
|
|
|
PDH complex, +
|
Ca2+, Pyruvate
|
|
|
PDH complex, -
|
acetyl CoA+NADH+
|
|
|
PFK-1, -
|
ATP, citrate
|
|
|
PFK1, +
|
AMP, fructose 2,6BP (most potent, via insulin)
|
|
|
properties of hexokinase
|
low Km, low Kmax
|
|
|
protein kinase A is activated via cAMP, which is regulated by
|
+ by glucagon, - by insulin
|
|
|
pyruvate carboxylase
|
pyruvate to OAA, anaplerotic to TCA
|
|
|
pyruvate kinase, +
|
fructose 1,6BP
|
|
|
pyruvate kinase, -
|
cAMP-dependent protein kinase A (through glucagon)
|
|
|
regulating enzymes of PDH
|
PDH kinase, PDH phosphatase
|
|
|
regulation of lactate dehydrogenase
|
pyruvate\lactate, NADH\NAD+
|
|
|
regulatory enzymes of glycolysis
|
hexokinase, phosphofructokinase, pyruvate kinase
|
|
|
SGLT, where
|
epithelial cells of intestine, renal tubules, choroid plexus
|
|
|
where does PDH function
|
mitochondrial matrix
|
|
|
where is glucokinase found
|
liver parenchymal cells, islet cells of pancreas
|
