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74 Cards in this Set
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anabolic state
mostly happens in liver a muscles synthesis of glycogen from glucose |
glycogenesis
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catabolic state
glycogen-phosphorylase cleaves glucose from glycogen --> which may then be converted to glucose-6-phosphate for glycolysis |
glycogenolysis
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glucose-6-phosphate + 2 ATP --> 2 pyruvate + 4ATP + 2 NADH2
pyruvate may move to transition reaction (aerobic) or lactate production (anaerobic) |
glycolysis
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oxygen present
1 pyruvate + 1 coenzyme A + NAD+ --> 1 Acetyl CoA + CO2 + 1NADH (doubled per glucose molecule) |
transition reaction
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enters citric acid cycle
product of transition reaction but can also be derived from fatty acid oxidation and from ketogenic amino acids |
acetyl CoA
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per turn of cycle in citric acid cycle...
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2 CO2
3 NADH 1 FADH2 1 ATP |
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each NADH in the ETC produces..
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2.5 ATP
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each FADH2 in the ETC produces...
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1.5 ATP
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net ATP gained from the ETC per glucose molecule
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28 ATP
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in anaerobic conditions, this reaction takes place to replace NAD+ which is necessary for reduction during glycolysis
pyruvate is converted to lactate through the oxidation of one NADH |
fermentation
anaerobic respiration 2ATP |
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lactate produced in the muscle during anaerobic respiration is sent to the liver
there it is converted to glucose through gluconeogenesis then sent back to muscle this process is called... |
cori cycle
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what enters the process of lipolysis
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triglycerides packaged inside lipoproteins, or triglycerides stored in adipose tissue
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acts for lipolysis in the muscle and adipose tissues
fatty acids are cleaved off of triglycerides in lipoproteins and taken up by the muscle or adipose tissues |
lipoprotein lipase (LPL)
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acts in adipose tissue
fatty acids are cleaved off triglycerides in the adipose tissue they are released into circulation and transported to tissues by the protein albumin the tissues use the fatty acids for fatty acid oxidation |
hormone-sensitive lipase (HSL)
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where are fatty acids oxidized?
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inside mitochondria
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in fatty acid oxidation inside the mitochondrion 2 C atoms of a fatty acid (ex. 18 C long) are cleaved off
this results in the formation of: |
1 acetyl-CoA
1 NADH 1 FADH2 |
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acetyl CoA moves from the mitochondrion into the cytosol
the addition of acetyl CoA is essentially repeated 7 times adding 2 carbons each time in total to form a 16 C fatty acid most fatty acids will be esterified into triglycerides |
de novo lipogenesis
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the rate limiting enzyme in cholesterol synthesis
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HMG-CoA reductase
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happens mostly in the liver and the small intestine
starts w/ acetyl CoA molecule through a series of enzymatic reactions, acetyl CoA is elongated and then cyclized to cholesterol |
cholesterol synthesis
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located in the endothelium (blood vessels)
cleaves fatty acids from chylomicrons and converts them to chylomicron remnants this operation is repeated for the subsequent lipoproteins up to LDL (chylomicron remnants --> VLDL --> IDL --> LDL) the fatty acids are taken up into the adipose and muscle tissue |
lipoprotein lipase
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located in the adipose tissue
glucagon and epinephrine stimulate the activity cleaves off fatty acids from the triglycerides stored in adipose cells these fatty acids are released into circulation, transported by the protein albumin and taken up by tissues (ex. muscle) for fatty acid oxidation insulin decreases the activity |
hormone-sensitive lipase
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absorption of fatty acids into the adipose cells is under the effect of LPL in this state
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fed state (anabolic)
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HSL releases fatty acids into circulation for energy production (fatty acid oxidation) in the tissues in this state
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mobilization / fasting (catabolic)
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long chain fatty acid cannot diffuse through the mitochondrial membrane
what facilitates this transport |
CPT enzymes and carnitine
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why are ketone bodies generated
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glucose is one of 2 energy sources for the brain
in its absence, the brain can use ketone bodies, instead of glucose |
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how are ketone bodies generated
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liver uses acetyl CoA (mostly from fatty acid oxidation but also some from ketogenic AAs) to synthesize ketone bodies
ketone bodies enter circulation and reach the brain brain coverts them to acetyl CoA --> citric acid cycle --> ATP |
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why can high levels of ketone bodies be a problem?
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a high concentration of ketone bodies in the blood results in ketoacidosis (low blood pH)
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drugs that inhibit HMG CoA reductase (limiting enzyme in cholesterol synthesis) in order to reduce the production of cholesterol
limiting cholesterol reduces the amount of LDL and therefore the risk of cardiovascular disease |
statins
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transfer of an amine group from an amino acid to a keto acid
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transamination
one of two possible initial steps of AA breakdown |
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removal of the amine group as ammonia (NH3)
formation of a keto acid and an ammonia molecule |
deamination
one of two possible initial steps of AA breakdown |
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AA is converted to pyruvate or citric acid intermediates
essentially glycolysis process happens in reverse w/ an oxaloacetate workaround |
gluconeogenesis from AAs
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AAs that are converted to acetyl CoA
acetyl CoA is used by the liver for ketogenesis or can be used in the citric acid cycle or in de novo lipogenesis and cholesterol synthesis |
ketogenic AAs
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occurs when citric acid cycle intermediates are depleated
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ketogenesis
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keto acid/carbon skeleton use in protein metabolism
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they are the base for synthesis of nonessential amino acids
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keto acid/carbon skeleton use in gluconeogenesis
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keto acids/carbon skeletons from glucagonic AAs will be converted to pyruvate or citric acid intermediates
they can enter gluconeogenesis |
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keto acid/carbon skeleton use in carbohydrate metabolism
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glucogonic AAs can be converted to either pyruvate or a citric acid cycle intermediate
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why is urea made
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amine group is removed as ammonia in deamination.. and too much ammonia in the blood results in hyperammonia
this must be excreted |
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how is urea made
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liver combines two molecules of ammonia and one CO2 to a molecule of urea
liver secretes urea into circulation kidneys excrete urea in urine |
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this type of AA is converted to pyruvate or citric acid cycle intermediates, essentially going through reverse glycolysis to produce glucose
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glucogenic AAs
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these AAs are converted to acetyl CoA or a ketone body precursor
acetyl CoA cannot participate in gluconeogenesis b/c the transition reaction is irreversible |
ketogenic AAs
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ethanol is converted to acetaldehyde by...
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alcohol dehydrogenase
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acetaldehyde is converted to acetyl-CoA by...
this produces 2 NADH |
aldehyde dehydrogenase
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when an individual consumes a large amount of alcohol, this system also converts ethanol to acetaldehyde
one molecule of NADPH is oxidized |
microsomal ethanol oxidizing system (MEOS)
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liver does all metabolic functions except for
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lactate synthesis
ketone body breakdown |
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vitamins A, D, E, K
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fat-soluble
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vitamins C and Bs
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water-soluble
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molecule that bears an unpaired electron in an outer shell orbital
these molecules are unstable and tend to complete their orbital by removing an electron from other molecules they can be endogenous or exogenous |
free radicals
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a free radical containing at least one oxygen atom
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reactive oxygen species
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imbalance b/t the production of reactive oxygen species and the body's antioxidant systems ability to quench them
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oxidative stress
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what minerals serve as cofactors for antioxidant enzymes?
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iron, copper, zinc, manganese
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what vitamins act as antioxidants?
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vitamins E and C
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antioxidant network
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once an antioxidant is oxidized by a free radical, the antioxidant is reduced back by another antioxidant in order to perform its function again
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what must be true of an antioxidant if it is to be meaningful?
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1. must be found in sufficient concentration at the correct location inside the body
2. cannot be redundant if an antioxidant is found in low amounts in a tissue along w/ another plentiful antioxidant that has similar antioxidant function, it is redundant |
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what is ORAC?
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oxygen radical absorbance capacity
these values show the ability of different antioxidants to reduce oxygen species of free radicals in vitro in vitro values may not reflect the bioactivity of the antioxidants in the body |
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vit E molecules w/ a saturated tail
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tocopherols
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vit E molecules w/ an unsaturated tail
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tocotrienols
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main form of vit E in the body
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alpha-tocopherrol
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americans consume large amounts of ________, however the most common form circulating in the body is________
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gamma-tocopherol
alpha-tocopherol |
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facilitates the insertion of vit E into VLDL in the liver
binds preferentially to 2R alpha-tocopherol as a result more 2R tocopherol molecules are in circulation than the other form of vit E |
alpha-tocopherol transfer protein
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each of the 3 stereocenters in the tail of this molecule of vit E is in the R configuration
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natural alpha-tocopherol
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a racemic mixture of the 8 possible configurations
combinations w/ R in pos 2 will bind preferentially to the alpha-tocopherol transfer protein |
synthetic alpha-tocopherol
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sets the recommended daily allowance (RDA) based upon the amount of 2R alpha-tocopherol present in a food
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DRI committee
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a unit that measures the bioactivity of a substance rather than the actual amount
used for vit A, D, E, C |
international unit (IU)
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represents the mg of alpha-tocopherol in one international unit
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conversion factor
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how does vit E possibly cause blood clotting problems?
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vit E metabolites interfere w/ the coagulating abilities of vit K
linked to decrease in blood clotting, hemorrhagic strokes in particular are linked |
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scientific name for reduced form of vit C
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ascorbic acid
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scientific name for vit C oxidized once
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semi-dehydroascorbate
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scientific name for vit C in fully oxidized form
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dehydroascorbate
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DHA is transported into the cell down its concentration gradient via facilitated diffusion using _____ or _____
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GLUT1 or GLUT3
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the essential building blocks of collagen
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hydroxylated lysine and proline
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hydroxylation of lysine and proline is carried out by the enzymes...
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lysyl hydroxylase and prolyl hydroxylase
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reduces Fe3+ back to Fe2+ so that enzymes can perform hydroxylation over and over
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vit C
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who was the chemist that obtained the nobel prize twice, that claimed high doses of vit C could protect against the common cold, cardiovascular disease, and cancer?
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Dr. Linus Pauling
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why could high levels of vit C increase the risk for kidney stones?
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high vit C intake increases excretion of both uric and oxalic acid, both of which are known components of kidney stones
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