Hn 400 Test 3

Front 1

anabolic state

mostly happens in liver a muscles

synthesis of glycogen from glucose

Back 1

glycogenesis

Front 2

catabolic state

glycogen-phosphorylase cleaves glucose from glycogen --> which may then be converted to glucose-6-phosphate for glycolysis

Back 2

glycogenolysis

Front 3

glucose-6-phosphate + 2 ATP --> 2 pyruvate + 4ATP + 2 NADH2

pyruvate may move to transition reaction (aerobic) or lactate production (anaerobic)

Back 3

glycolysis

Front 4

oxygen present

1 pyruvate + 1 coenzyme A + NAD+ --> 1 Acetyl CoA + CO2 + 1NADH

(doubled per glucose molecule)

Back 4

transition reaction

Front 5

enters citric acid cycle

product of transition reaction but can also be derived from fatty acid oxidation and from ketogenic amino acids

Back 5

acetyl CoA

Front 6

per turn of cycle in citric acid cycle...

Back 6

2 CO2
3 NADH
1 FADH2
1 ATP

Front 7

each NADH in the ETC produces..

Back 7

2.5 ATP

Front 8

each FADH2 in the ETC produces...

Back 8

1.5 ATP

Front 9

net ATP gained from the ETC per glucose molecule

Back 9

28 ATP

Front 10

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

Back 10

fermentation

anaerobic respiration 2ATP

Front 11

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...

Back 11

cori cycle

Front 12

what enters the process of lipolysis

Back 12

triglycerides packaged inside lipoproteins, or triglycerides stored in adipose tissue

Front 13

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

Back 13

lipoprotein lipase (LPL)

Front 14

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

Back 14

hormone-sensitive lipase (HSL)

Front 15

where are fatty acids oxidized?

Back 15

inside mitochondria

Front 16

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:

Back 16

1 acetyl-CoA
1 NADH
1 FADH2

Front 17

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

Back 17

de novo lipogenesis

Front 18

the rate limiting enzyme in cholesterol synthesis

Back 18

HMG-CoA reductase

Front 19

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

Back 19

cholesterol synthesis

Front 20

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

Back 20

lipoprotein lipase

Front 21

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

Back 21

hormone-sensitive lipase

Front 22

absorption of fatty acids into the adipose cells is under the effect of LPL in this state

Back 22

fed state (anabolic)

Front 23

HSL releases fatty acids into circulation for energy production (fatty acid oxidation) in the tissues in this state

Back 23

mobilization / fasting (catabolic)

Front 24

long chain fatty acid cannot diffuse through the mitochondrial membrane

what facilitates this transport

Back 24

CPT enzymes and carnitine

Front 25

why are ketone bodies generated

Back 25

glucose is one of 2 energy sources for the brain

in its absence, the brain can use ketone bodies, instead of glucose

Front 26

how are ketone bodies generated

Back 26

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

Front 27

why can high levels of ketone bodies be a problem?

Back 27

a high concentration of ketone bodies in the blood results in ketoacidosis (low blood pH)

Front 28

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

Back 28

statins

Front 29

transfer of an amine group from an amino acid to a keto acid

Back 29

transamination

one of two possible initial steps of AA breakdown

Front 30

removal of the amine group as ammonia (NH3)

formation of a keto acid and an ammonia molecule

Back 30

deamination

one of two possible initial steps of AA breakdown

Front 31

AA is converted to pyruvate or citric acid intermediates

essentially glycolysis process happens in reverse w/ an oxaloacetate workaround

Back 31

gluconeogenesis from AAs

Front 32

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

Back 32

ketogenic AAs

Front 33

occurs when citric acid cycle intermediates are depleated

Back 33

ketogenesis

Front 34

keto acid/carbon skeleton use in protein metabolism

Back 34

they are the base for synthesis of nonessential amino acids

Front 35

keto acid/carbon skeleton use in gluconeogenesis

Back 35

keto acids/carbon skeletons from glucagonic AAs will be converted to pyruvate or citric acid intermediates

they can enter gluconeogenesis

Front 36

keto acid/carbon skeleton use in carbohydrate metabolism

Back 36

glucogonic AAs can be converted to either pyruvate or a citric acid cycle intermediate

Front 37

why is urea made

Back 37

amine group is removed as ammonia in deamination.. and too much ammonia in the blood results in hyperammonia

this must be excreted

Front 38

how is urea made

Back 38

liver combines two molecules of ammonia and one CO2 to a molecule of urea

liver secretes urea into circulation

kidneys excrete urea in urine

Front 39

this type of AA is converted to pyruvate or citric acid cycle intermediates, essentially going through reverse glycolysis to produce glucose

Back 39

glucogenic AAs

Front 40

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

Back 40

ketogenic AAs

Front 41

ethanol is converted to acetaldehyde by...

Back 41

alcohol dehydrogenase

Front 42

acetaldehyde is converted to acetyl-CoA by...

this produces 2 NADH

Back 42

aldehyde dehydrogenase

Front 43

when an individual consumes a large amount of alcohol, this system also converts ethanol to acetaldehyde

one molecule of NADPH is oxidized

Back 43

microsomal ethanol oxidizing system (MEOS)

Front 44

liver does all metabolic functions except for

Back 44

lactate synthesis
ketone body breakdown

Front 45

vitamins A, D, E, K

Back 45

fat-soluble

Front 46

vitamins C and Bs

Back 46

water-soluble

Front 47

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

Back 47

free radicals

Front 48

a free radical containing at least one oxygen atom

Back 48

reactive oxygen species

Front 49

imbalance b/t the production of reactive oxygen species and the body's antioxidant systems ability to quench them

Back 49

oxidative stress

Front 50

what minerals serve as cofactors for antioxidant enzymes?

Back 50

iron, copper, zinc, manganese

Front 51

what vitamins act as antioxidants?

Back 51

vitamins E and C

Front 52

antioxidant network

Back 52

once an antioxidant is oxidized by a free radical, the antioxidant is reduced back by another antioxidant in order to perform its function again

Front 53

what must be true of an antioxidant if it is to be meaningful?

Back 53

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

Front 54

what is ORAC?

Back 54

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

Front 55

vit E molecules w/ a saturated tail

Back 55

tocopherols

Front 56

vit E molecules w/ an unsaturated tail

Back 56

tocotrienols

Front 57

main form of vit E in the body

Back 57

alpha-tocopherrol

Front 58

americans consume large amounts of ________, however the most common form circulating in the body is________

Back 58

gamma-tocopherol

alpha-tocopherol

Front 59

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

Back 59

alpha-tocopherol transfer protein

Front 60

each of the 3 stereocenters in the tail of this molecule of vit E is in the R configuration

Back 60

natural alpha-tocopherol

Front 61

a racemic mixture of the 8 possible configurations

combinations w/ R in pos 2 will bind preferentially to the alpha-tocopherol transfer protein

Back 61

synthetic alpha-tocopherol

Front 62

sets the recommended daily allowance (RDA) based upon the amount of 2R alpha-tocopherol present in a food

Back 62

DRI committee

Front 63

a unit that measures the bioactivity of a substance rather than the actual amount

used for vit A, D, E, C

Back 63

international unit (IU)

Front 64

represents the mg of alpha-tocopherol in one international unit

Back 64

conversion factor

Front 65

how does vit E possibly cause blood clotting problems?

Back 65

vit E metabolites interfere w/ the coagulating abilities of vit K

linked to decrease in blood clotting, hemorrhagic strokes in particular are linked

Front 66

scientific name for reduced form of vit C

Back 66

ascorbic acid

Front 67

scientific name for vit C oxidized once

Back 67

semi-dehydroascorbate

Front 68

scientific name for vit C in fully oxidized form

Back 68

dehydroascorbate

Front 69

DHA is transported into the cell down its concentration gradient via facilitated diffusion using _____ or _____

Back 69

GLUT1 or GLUT3

Front 70

the essential building blocks of collagen

Back 70

hydroxylated lysine and proline

Front 71

hydroxylation of lysine and proline is carried out by the enzymes...

Back 71

lysyl hydroxylase and prolyl hydroxylase

Front 72

reduces Fe3+ back to Fe2+ so that enzymes can perform hydroxylation over and over

Back 72

vit C

Front 73

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?

Back 73

Dr. Linus Pauling

Front 74

why could high levels of vit C increase the risk for kidney stones?

Back 74

high vit C intake increases excretion of both uric and oxalic acid, both of which are known components of kidney stones