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49 Cards in this Set

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Know the reactions and the enzymes in glycolysis
glucose to to glu-6-P via hexokinase, (commits to metabolism in cell) glu-6-p to fru -6-p via phosphoglucose isomerase,
PFK-1: F-6-P to F-1,6-bisP(1st commited step, req ATP)
Aldolase cleaves
into dihydroxyacetone phosphate (DHAP) and glyceraldehyde 3-P
Triose phosphate isomerase converts DHAP into GALD-3-P,
GlycAld-3-P DH into 1,3 BisPGlycerate,
phosphoglycerate kinase into 3PGlcrate +ATP
pho-g-ate mutase into 2 P-G-ate
enolase into PEP and H2O
Pyruvate kinase into pyruvate and ATP
Net Reaction glyclolysis
Glucose + 2NAD+ + 2Pi + 2ADP → 2Pyruvate + 2NADH + 4H+ + 2ATP + 2H2O
digestion of starch
begins in mouth with alpha-amylase: starch → alpha-dextrins
Pancreatic alpha-amylase continues digestion into maltose and maltotriose and limit dextrins,
At the microvilli:
Glucoamylase hydrolyses alpha-1,4 of dextrins
Sucrase-isomaltase-sucrose, maltose,isomaltose
Beta-glycosidase-lactose, glycolipids
conversion of glucose to glucose-6-phosphate
hexokinase (glucokinase in liver), commits glucose to to metabolism in that cell, uses ATP, high negative delta G
What is Glycogenin? What is its role?
glycogenin autoglycosylates by attaching UDP-G to a Ser -OH, then extends chain, its a primer for adding glucose monomers
Understand glycogen chain elongation
Glycogen synthase is the regulated step, Glucosyl residues added from UDP-G to nonreducing ends
Anomeric C attached in alpha-1,4 to -OH of C4 of terminal glucosyl
When chain reaches 11, a 6-8 piece is cleaved by amylo-4:6-transferase and reattached to a glucosyl by an alpha-1,6 bond
How are Galactose and Fructose metabolized?
Fructose:phosphorylation by fructokinase → fructose-1-P → cleaved by aldolase B to DHAP +glyceraldehyde, →Glhyde3P via triose kinase →→→Pyruvate
Galactose:Glactokinase→galactose1P→Gal1P uridylyltranferase→Glucose-1-P→Glucose 6-P
How are erythrocytes protected against hemolysis?
hexose monophosphate shunt (first step enzyme glucose 6 Phosphate Dehydrogenase, G6PD) produces NADPH, maintaining Glutathione (defense against reactive Oxygen species)
the oxidative branch of the pentose phosphate pathway
G-6-P is oxidatively decarboxylated to ribulose-5-P :G-6-P dehydrogenase oxidizes the aldehyde at C1 and reduces NADP+ to NADPH,
Gluconolactone rapidly hydrolyzed to 6-phosphogluconate,Next oxidation releases CO2 with the electrons being transferred to NADP+, 2 NADPH per glucose
compare mitochondrial versus peroxisomal pathways of the Beta-oxidation spiral during fatty acid metabolism
peroxyzomes can do VLCFA's, make make H2O2, stops at 4-6 C's, enter without carnitine.
understand the synthesis of lactose
Lactose is synthesized from UDP-galactose + glucose, only in mammary gland,Lactose synthase (alpha- lactabumin+ galactosyltranferase) catalyzes transfer of galactose from UDP-galactose to glucose, alpha- lactabumin (stim. by prolactin) subunit lowers Km (increases production), without it ya get glycoprotiens.
glutathione
composed of glu, cys & gly, reduced by NADPH,made primarily in liver,
Used to detoxify free radicals, including:
acetalaldehyde (EtOH)
NAPQI (acetomeniphen),
radical Oxygen species in RBC's,
Vinyl Chloride,
pyruvate carboxylase reaction
with biotin, using ATP, adds a CO2 to pyruvate to form Oxaloacetate, stimulated by Acetyl CoA, Active in Gluconeogenisis, FA synthesis.
gluconeogenesis -- key enzymes, key steps and where does it take place within the cell
In the liver, made from lactate, glycerol AA's ( prim alanine), stimulated by epinephrine,3 steps dif. than reverse glycolysis. Pyruvate+CO2 to OAA via Pyruvate carboxylase and Biotin in mito, phosphoenolpyruvate carboxykinase takes CO2 off to make PEP (GTP used)cytosol, then dephosporylation of F1,6bisP, and Glu 6P(cytosol) OAA can't cross mito mem.
long term starvation conditions
brain starts using ketones, liver can't use ketones, gluconeogenisis decreases but even after 5 wk. starvation, Blood glucose is still 65. reduced GLUT4 in muscle, stimulates GH
transport of dietary triacylglycerols
bile salts emulsify, but remain in lumen as free FA's cholesterol, glycerol cross membrane, packaged in chylomicrons (apo48), though lymph, eventually liver uses them or repackages into VLDL(apo100)
chylomicrons
Intestinal cells package TAGs , proteins, and phosoplipids with cholesterol, and apoprotien B-48,Nascent chylos receive apoE(liver recog) and apoCII(LPL activation) from HDL.
Now mature, TAGs digested by LPL @ adipose and muscle, remnant binds apo E recep in hepatocytes, endocytosed and degraded
the fatty acid synthase reaction
composed of two identical dimers, each have 7 catalytic activities  and an acyl carrier protein (ACP) segment(contains a phosphopantetheine from coenzyme A), in cytosol, adds 2 C units from malonyl CoA to the chain, uses 2 NADPH after addition >> palmitate (c16)
formation of malonyl CoA
acetyl CoA carboxylase adds a carboxyl group to acetyl CoA in a reaction requiring biotin and ATP,
A high insulin/glucagon ratio>>induction of the synthesis of both acetyl CoA carboxylase and fatty acid synthase
endogenous antioxidants
Endogenous uric acid from degradation of purines: blood, saliva, lung lining fluid
Endogenous melatonin from pineal gland can undergo suicidal transformation
SuperOxideDismutase, SOD, catalase, glutathione peroxydase, H2O2 killers
cholesterol synthesis
All of the 27 carbons are derived from acetyl CoA, requires NADPH
Acetyl CoA to Mevalonate via HMG-CoA synthase and reductase
Mevalonate to dimethylallyl pyrophosphate via tons of ATP
then to gerenal phosphate(10C) to farnesyl(15C) to Sqalene (30C)>>>>Cholesterol
synthesis of bile acids
amphipathic,act as detergents,synthesized in the liver,derived from cholesterol-contain more hydroxyl groups and a polar side chain, and lack a 5-6 double bond, recycled
formation of leukotrienes
start with Arachidonic acid to hydroperoxyeicosatetraenoic acids (HPETEs),
major leukotrienes are produced by 5-lipoxygenase
mast cells make leukotriene A4 (LTA4)
enzymes for platelet aggregation
factor XIIIa (fibrin crosslinking)
VII, XI, IX, X, XII, and prothrombin

anti agg: Prostaglanins and NO
Aspirin and ibuprofen metabolism
major is salicylurate, and hippate excreation for aspirin
MEOS
Ethanol to acetaldehyde by CYP2E1, Ethanol & NADPH both donate e-,2 components: electon donating reductase and cytochrome P450
CYP2E1: inducible, high Km, may produce acetaldehyde faster than can be metabolized and can generate free radicals
products of alcohol metabolism
alcohol go through AlcoholDH (and CYP2E1, needs NADPH) to acetalaldahyde to acetate via acetalaldahyde DH to acetyl CoA via acetyl CoA synthetase, Ketoacidosis, fatty liver, etc.
Pepsinogen
Chief cells stomach, works in low pH, self cleaved in acid environment (stomach)
trypsinogen and chymotrypsinogen
act as endopeptidases:
trypsinogen to trypsin via enteropeptidase secreted by the brush-border cells>>>cleaves dietary proteins and activates other digestive proteases chymotrypsinogen:Chymotrypsin favors residues that contain hydrophobic or acidic amino acids
What is Ubiquitin
labels proteins for proteasomal degradation, uses ATP
What is Urea, how is it formed?
NH4+, bicarbonate, and the nitrogen of aspartate

NH4+, bicarbonate, and ATP produce carbamoyl phosphate which reacts with ornithine to form citrulline,add aspartate=argininosuccinate, which releases fumarate, forming arginine, cleave arginine(arginase), you get Urea and ornathine
what are the mitochondrial enzymes of the urea cycle?
carbamoyl phosphate synthase I and ornithine transcarbamoylase
understand Pyridoxal phosphate
Vit B6, all transamination rxns,
deficiency can result in homocystinemia This little guy gets around!
how does allopurinol treat gout?
blocks xanthine oxidase stops uric acid gout
glycine and serine metabolism-
The major route from serine is by a reversible reaction that involves FH4 and pyridoxal phosphate.
what is S-adenosyl methionine? What is it used for?
produced from methionine and adenosine triphosphate (ATP), transfers the methyl group to precursors forming a number of compounds, including creatine, phosphatidylcholine, epinephrine, melatonin, methylated nucleotides, and methylated DNA.
red blood cells general features-
biconcave, NADH reduces Methinonine, NADPH made from shunt to keep Glutathinone working, 120 life cycle, spectrin, ankyrin, and band 3 make up cytoskeleton. has hemoglobin
removal of ammonia in the brain-
glutamine gets rid of the NH4+
key reactions of heme synthesis
Heme is synthesized from glycine and succinyl CoAform -aminolevulinic acid (delta?gamma?-ALA).2 condense to form the pyrrole, prophobilinogen.Four of these pyrrole rings condense iron (as Fe2+) is incorporated into protoporphyrin IX by ferrochelatase.
Acetaminophen (Tylenol) metabolism-
NAPQI, glutathione, High EtOH= to much cytochrome=too much NAPQI= liver damage
Protein C and protein S working as anticoagulants -- understand how this works-
Protein C and its cofactor protein S serve to suppress the activity of the coagulation cascade.
Protein S anchors the activated protein C complex (APC) to the clot through Ca2+/-carboxyglutamate binding to platelet phospholipids.
The APC destroys the active blood coagulation cofactors Factor VIIIa and Factor Va.
This decreases the production of thrombin.
APC also stimulates endothelial cells to increase secretion of the prostaglandin PGI2, which reduces platelet aggregation.
formation of -carboxyglutamic acid residues-
formation of blood coagulation factor takes place in the hepatocyte before release of the protein, vitamin K req
what are the roles of Albumin?- transport, osmotic factors,
Approximately 60% of the total plasma protein is thought to contribute 70 to 80% of the total osmotic pressure of the plasma.
It is a glycoprotein and is a carrier of free fatty acids, calcium, zinc, steroid hormones, copper, and bilirubin.
When a drug binds to albumin, such binding will likely lower the effective concentration of that drug and may lengthen its lifetime.
differences between the liver and other tissues in the glucose utilization-
The rate of glucose utilization by the liver is determined in part by the activity of glucokinase.glucose will enter liver principally after its concentration raises in the portal blood (10-40 mM), and not at the lower 5 mM in hepatic artery
role of AMP in muscles
-Increased AMP levels activate PFK-1 and glycogenolysis, providing additional ATP from anaerobic glycolysis. AMP is an ideal activator because its concentration is normally kept low by adenylate kinase equilibrium [2ADP ↔ AMP + ATP].
Anaerobic glycolysis in muscle
-Fast twitch IIb, low hexokinase levels, relies on endogenous glycogen and creatine phosphate, PFK-1 activated and starts glycogenolysis
glycogen synthesis in skeletal muscle-
at rest, with high ATP levels, PFK inactive, ect, insulin stimulated?
role of Ca2+ in muscles
-calcium ion and ATP remain available, the myosin heads will contract, Ca also activates glycogen phosphorylase b, increasing glycogenolysis
the Cori cycle
- lactate to glucose in the liver, prevention of lactic acidosis