Nutr 470 Final Exam

Front 1

carbohydrates - DRI values

Back 1

1. RDA = 130g/day (brains needs)
2. AMDR=45-65% (low end-AI for fiber, high end-hypertriglyceremia)
3. AI fiber = 38 g/day men, 30 g/day women
4. added sugars < 25% kcal

Front 2

carbohydrates - dietary guidelines

Back 2

1. increase fruit/veg, whole grain, non-fat/low-fat dairy
2. 3 servings whole grain
3. decrease discretionary calorie intake

Front 3

fats - DRI values

Back 3

1. NO RDA/AI for total fat
2. AMDR = 20-35% (low-carb intake too high; high-AI fiber, obesity)
3. AI linoleic = 17g/day men, 12 g/day women
AI linolenic = 1.6g/day men, 1.1 g/day men
4. cholesterol, sat fat, and trans fat as low as possible

Front 4

proteins - DRI values

Back 4

1. RDA = .8g/kg body weight (for essential AAs-based on N-balance studies)
2. AMDR = 10-35% (low-essential AA req; high- AI fiber, fat intake too low)
3. Requirements for source of essential AAs and nitrogen
4. high quality programs (all essential, right proportions, digestable)

Front 5

digestion - mouth

Back 5

starch -(salivary amylase)-> maltose

Front 6

digestion - stomach

Back 6

carbs: salivary amylase inactivated (low pH)

proteins: HCl denatures proteins;
pepsinogen (inact)-(HCL)->pepsin (act)
proteins -(pepsin)->smaller PPs

Front 7

digestion - small intestine

Back 7

carbs: starch -(pancreatic amylase)-> maltose [secreted by pancreas through duct to duodenum)
lac/mal/suc->MSs (in microvilli)

fats: TGs -(pancreatic lipase)-> 2 FFAs + 1 monoglyceride
**when fat enters SI, cholecystekinen secreted/triggers gallbladder to release bile (made in liver)

Front 8

digestion - large intestine

Back 8

carbs: dietary fiber -(fermentation)-> SCFA, menthane, CO2, H2

Front 9

carbohydrates - absorption

Back 9

MSs absorbed from GI tract; go into blood/lymph

apical membrane: glucose/galactose-active trans (SGLT1); fructose-fac diff (GLUT5)

basolateral membrane: all 3-fac diff (GLUT2)

once absorbed in GI cells, go through portal vein to liver (fruc-metabolized/converted to gluc; sucr-converted to gluc)

Front 10

lipids - absorption

Back 10

micelles (LCFAs>10 Cs) absorbed into intestinal mucosal cells

SCFAs directly absorbed; go through portal vein-->liver

Front 11

lipids - transportation

Back 11

chylomicrons form from dietary TGs; released by exocytosis into lymph system; go through thoracic duct-->blood

VLDL - transport synthesized TGs

Front 12

proteins - absorption/transportation

Back 12

end products = free AAs, DPs, TPs, oligopeptides

transportation = active transport
acidic AAs, neutral AAs, phenylalanine/methionine, proline/hydroxyproline

Front 13

carbohydrates - 4 components

Back 13

1. basal metabolism - energy expenditure needed to maintain bio. fxns); 30% ion trans
2. physical activity
3. heat increment - expenditure due to digestion; 5%BMR + activity
4. growth (incr body mass, preg, lactation)

Front 14

ATP regeneration (2 rxns)

Back 14

1. substrate-level phosphorylation

2. oxidative phosphorylation - substrate oxidized/coenzyme reduced, then passes e's to ETS to generate ATP

Front 15

substrate-level phosphorylation

Back 15

In glycolysis:
1,3-BPG+ADP-->3-PG+ATP
PEP+ADP-->Pyruvate+ATP

In TCA cycle:
succinyl coA+ADP-->succinate+ATP

Front 16

oxidative phosphorylation

Back 16

substrate oxidized
coenzyme reduced (NAD-->NADH + H)
coenzyme passes e's into ETS to generate ATP

ex: GAP+NAD-->1,3-BPG+NADH+H

Front 17

importance of glucose (4)

Back 17

1. used by every cell
2. only E-source for RBCs
3. only anaerobic E-source
4. only E-source for brain/nervous tissue (except during starvation)

Front 18

requirements for glucose to enter cells (3)

Back 18

1. facilitated diffusion - needs transporter (insulin= +muscle/adipose, -brain/liver uptake)
2. go down concentration gradient
3. activated glucose (glu-6-P)

Front 19

HK vs. GK

Back 19

HK-when blood glucose LOW
location=all cells except liver
Km=10^5 (higher affinity)
Vmax=low
inhibitors=glu-6-P

GK-when blood glucose HIGH
location=liver
Km=10^-2 (low affinity)
Vmax=high affinity
no inhibitors

Front 20

glycolysis - overall rxn

Back 20

glucose + 2 ATP + 2 NAD --> pyruvate(aerobic)/lactate(anaerobic) + 4 ATP + 2 NADH + H

Front 21

glycolysis - energy loss rxns (2)

Back 21

1. glucose -(HK)-> glucose-6-P

2. fructose-6-P -(PFK1)-> fructose-1,6-BP

total loss=2 ATP

Front 22

glycolysis - energy gain rxns (2)

Back 22

1. 1,3-BPG-(PGK)->3-PG

2. PEP-(PK)->pyruvate

total gain=4 ATP

Front 23

regulation of glycolysis - PFK1

Back 23

negative = ATP, citrate

positive = AMP/ATP, fructose-6-P, fructose-1,6-BP (made by PFK2, activated by F-6-P)

Front 24

regenerating coenzymes (3)

Back 24

1. oxidation of GAP:
GAP+NAD-(GAP DH)-> 1,3-BPG+NADH

2. regenerating NAD+ anaerobically
pyruvate+NADH-->lactate+NAD

3. regenerating NAD+ aerobically
a)malate shuttle
b)glycerol-3-P shuttle

Front 25

malate shuttle

Back 25

in cytosol:
OAA-->Malate
NADH-->NAD

in mitochondria:
Malate-->OAA
NAD-->NADH

ATP=3

Front 26

glycerol-3-P shuttle

Back 26

in cytosol:
DHAP-->glycerol-3-P
NADH-->NAD

in mitochondria:
glycerol-3-P-->DHAP
FAD-->FADH2

ATP=2

Front 27

4 pathways of pyruvate

Back 27

1. alanine
2. lactate (anaerobic glycolysis)
3. acetyl coA
4. oxaloacetate (gluconeogenesis)

Front 28

oxidative decarboxylation of pyruvate - rxn

Back 28

pyruvate + CoA-SH--(PDH complex)-->acetyl coA + CO2

Front 29

oxidative decarboxylation of pyruvate - enzymes

Back 29

1. TPP (vitamin=thiamin) - allows for decarboxylation of pyruvate
2. CoA (vitamin=pantothenic acid) - picks up 2C unit from lipoic acid
3. FAD (vitamin=riboflavin) - accepts e-s from lipoic acid
4. NAD (niacin) - accepts e-s from FADH2 and donates to ETS

Front 30

oxidative decarboxylation of pyruvate - steps

Back 30

1. TPP binds to pyruvate, allowing it to be decarboxylated
2. acetyl group transferred to lipoamide-->acetyllipoamide
3. CoA picks up acetyl group from acetyl lipoamide (acetyl coA)
4. e-s from lipoic acid transferred to FAD (-->FADH2)
5. e-s from FADH2 transferred to NAD (-->NADH)
6. NADH transfers e-s to ETS

Front 31

oxidative decarboxylation of pyruvate - regulation

Back 31

kinase (-):
pos-acetyl coA/NADH
neg-NAD

phosphatase (+)
pos-insulin
neg-acetyl coA/NADH

Front 32

TCA cycle - energetics

Back 32

1 substrate level phosphorylation (succinyl coA+GDP-->succinate+GTP)

3 NADH+H

1 FADH2

total ATP=12

Front 33

TCA cycle - overall reaction

Back 33

GDP + acetyl coA + coNZ --> GTP + 2 CO2 + coNZ-H

Front 34

TCA cycle - important reactions (2)

Back 34

1. OAA+acetyl coA--(citrate synthase)-->citrate
neg-lack of OAA

2. isocitrate+NAD --(ICDH)-->alpha-KG+NADH+H
neg-NADH

Front 35

TCA cycle and ETS

Back 35

important=maintaining energy balance in cell

key reg enzyme (TCA cycle)= ICDH

build up of NADH---->glucose cant get into cell

Front 36

lipoprotein lipase - fxn/location

Back 36

fxn- liberates TGs from lipoproteins
location-walls of blood capillaries

Front 37

lipoprotein lipase - Km/effectors

Back 37

Km:
heart/breast(lactation)= low Km for LPL
adipose= high Km for LPL

effectors:
glucose/insulin:
+ on adipose LPL
- on heart/skeletal LPL

glucagon:
- on adipose LPL
+ on heart/skeletal LPL

Front 38

lipids as energy source

Back 38

heart and liver - almost always use FAs for E

muscle - uses FAs when it can

brain cant use FAs for E

Front 39

sources of FAs for energy (2)

Back 39

1. dietary- FAs picked up by chylomicrons and used for E

2. adipose tissue (energy low)- TGs--(HSL)-->glycerol + FFAs
pos-glucagon/epinephrine
neg-insulin
**FFAs released and travel into blood bound to albumin

Front 40

beta oxidation - overall reaction

Back 40

palmitate+2ATP+8CoA+7NAD+7FAD ----> 8 acetyl coA+2ADP+7FADH2+7NADH+H

Front 41

beta oxidation - energetics/regulation

Back 41

energetics:
7 NADH, 7FADH2, 2 used=33 ATP

regulation:
1. availability of O
2. availability of FAs (diet/adipose)
3. oxidized cofactors (NAD/FAD)

Front 42

beta oxidation - sparing glucose

Back 42

1. produces NADH + H (inhibits ICDH, builds up citrate, spills out....glucose cant go into cell)

2. produces acetyl coA (inhibits pyruvate DH, aCoA-nongluconeogenic)

Front 43

ketone bodies - types

Back 43

made in liver

types:
1.beta-OH butyrate (urine)
2. acetoacetate (urine)
3. acetate (in breath)

Front 44

ketone bodies - conditions

Back 44

1. HSL activated (+glucagon/epinephrine)
2. beta oxidation activated (FAs/oxygen available, oxidized coenzymes)
3. body unable to get into TCA cycle (no OAA for acetyl coA to react w/)

Front 45

glycogen synthesis - reactions (3)

Back 45

mainly muscle/liver

1. glucose--(HK)-->glu-6-P
2. glu-6-P--->UDP-glucose
3.**UDP-glucose+glycogen(n)--(glycogen synthase)-->glycogen (n+1)

Front 46

glycogen synthesis - regulation

Back 46

1. covalent modification
kinase (-)
phosphatase (+)

2. hormonal
glucagon (-)
insulin (+)

3. allosteric
glucose-6-P (+)
glycogen (-)

Front 47

glycogen degredation - overall rxn/regulation

Back 47

glycogen(n)--(glycogen phosphorylase)-->glycogen(n-1)+glucose-1-P

1. covalent modification
kinase (+)
phosphatase (-)

2. hormonal
glucagon (+)
insulin (-)

3. allosteric
ADP/ATP (+)
glucose-6-P (-)

Front 48

TG synthesis - location/requirements

Back 48

location=liver (packaged/sent out in bood) and adipose (stored as TGs)

requirements:
1. glycerol-3-P
a)glycerol--(glycerol kinase)-->glycerol-3-P [not in adipose]
b)DHAP-->glycerol-3-P

2. FAs (FA synthesis rxn)

Front 49

fatty acid synthesis - overall reaction

Back 49

acetyl CoA + 7 malonyl CoA + 14 NADPH + H --(FA synthase)--> Palmitate + 8 CoA + 7 CO2 + 6 H20 + 14 NADP

*insulin increases amts of FA synthase

Front 50

fatty acid synthesis - source of acetyl CoA

Back 50

1. formation of citrate (mitochondria)
2. formation of acetyl coA (cytosol)
citrate --(citrate lyase)--> acetyl coA + OAA
pos-citrate

Front 51

fatty acid synthesis - source of malonyl coA

Back 51

in cytosol:
acetyl coA+CO2 --(acetyl coA carboxylase)--> malonyl coA
pos-citrate(potent)/ insulin
neg-LCFacyl CoA, glucagon/epinephrine

Front 52

fatty acid synthesis - source of NADPH

Back 52

1/2:
malate+NADP --(malic enzyme)--> pyruvate+CO2+NADPH+H

[source of malate: citrate --(citrate lyase)--> acetyl coA + OAA; OAA-->malate]

1/2: glucose-6-P DH (in HMP)

Front 53

fate of AAs (4)

Back 53

1. oxidation (AA-->pyr/acetyl coA/into TCA cycle)
2. glucose synthesis
3. protein synthesis
4. other N-containing compounds

Front 54

urea synthesis - reaction

Back 54

nitrogen primarily excreted as urea in urine

Aspartate+HCO3+3ATP+NH4+NH3 --->urea+fumarate+2ADP+2Pi+AMP+PPi

Front 55

urea synthesis - uses up...(5)

Back 55

1. HCO3-
2. H20
3. 4 ATP
4. NH4
glutamate+NAD--(glutamate DH)-->alpha-KG+NADH+NH4
5. NH3 (aspartate)

Front 56

transamination - alpha keto acids and their AAs

Back 56

1. glutamate/alpha-KG
2. aspartate/OAA
3. alanine/pyruvate

Front 57

transamination - GOT/GPT

Back 57

alpha-KG+aspartate--(GOT)-->glutamate+OAA

alpha-KG+alanine--(GPT)-->glutamate+pyruvate

**always start rxns with alpha-KG

Front 58

deamination reactions (4)

Back 58

1. NH4 lost in urine (kidneys)
glutamine--(glutaminase)-->glutamate+NH4

2. captured in urea cycle (liver)
glutamate--(glutamate DH)-->alpha-KG+NH4; NH4 to urea cycle

3. captured as glutamate (muscles)
alpha-KG+NH4+NAD ---> glutamate+NADH

4. captured in glutamine (muscles)
glutamate+NH4--(glutamine synthase)-->glutamine

Front 59

significance of transamination/deamination rxns

Back 59

1. detoxification
dietary surplus- N eliminated via trans/deamination rxns or urea formation

2. energy production
dietary surplus- C-skeletons conserved as FAs (FA synthesis-lipogenesis)
fasting- AAs-->glucose (GN)

Front 60

gluconeogenesis - enzymes (4)

Back 60

1. pyruvate carboxylase (bypasses PK)
2. PEPCK (bypasses PK)
3. FDP'ase (bypasses PFK-1)
4. G6P'ase (bypasses HK/GK)

Front 61

gluconeogenesis - controls

Back 61

pos - citrate, insulin

neg - F-2,6-BP, F-6-P, AMP/ATP

glucose (-) for G6Pase
acetyl coA (+) for glutamate DH

Front 62

carbs as glucose precursors

Back 62

carbs:
(in muscle) glycogen-->glu-1-P-->glu-6-P-->lactate
(in liver) lactate-->pyruvate-->gluconeogenesis-->GLUCOSE

Front 63

proteins/lipids as glucose precursors

Back 63

proteins-leucine/lysine only nongluconeogenic AAs

lipids:
(in adipose) TGs--(HSL)-->FFAs+glycerol
(in liver) glycerol--(glycerol kinase)-->glycerol-3-P
glycerol-3-P--(gly-3-P DH)-->DHAP-->gluconeogenesis-->GLUCOSE

Front 64

glucose/alanine cycle - transamination to remove N to break down proteins

Back 64

in muscle:
1. AA "X" + alpha-KG --> KA "X" + glutamate
2. glutamate + pyruvate --(GPT)-->alpha-KG+alanine
3. alanine-->liver

in liver:
4. alanine+alpha-KG--(GPT)-->pyruvate+glutamate
a)pyruvate-->gluconeogenesis-->GLUCOSE
b)glutamate+NAD--(glutamate DH)-->alpha-KG+NH4+NADH+H [NH4-->to urea cycle]

Front 65

glucose/alanine cycle - deamination to remove N to break down proteins

Back 65

in muscle:
1. alpha-KG+NH4+NADH+H--->glutamate+NAD
2. glutamate+NH3--(glutamine synthase)-->glutamine

In kidney:
3. glutamine --(glutaminase)-->glutamate+NH4 [NH4-out in urine]

Front 66

glucose/alanine cycle - gluconeogenesis in liver

Back 66

1. alanine (from muscle) enters liver
2. alanine+alpha-KG--(GPT)-->glutamate+pyruvate
a)pyruvate-->gluconeogenesis-->GLUCOSE
b)glutamate+NAD--(glutamate DH)-->alpha-KG+NH4+NADH
glutamate+OAA--(GOT)-->alpha-KG+aspartate [aspartate gives NH3 to urea cycle]

Front 67

fasting - glycogen degradation in liver

Back 67

in liver (releases free glucose into blood-G6Pase)
1. glycogen--(glycogen phosphorylase)-->glycogen(n-1)+glucose-1-P

2. glucose-1-P-->glucose-6-P
3. glucose-6-P--(G6P'ase)-->glucose+Pi [not in muscle]

Front 68

fasting - glycogen degradation in muscle

Back 68

1. glycogen--(glycogen phosphorylase)-->glycogen(n-1)+glucose-1-P
2. glucose-1-P-->glucose-6-P
3. glucose-6-P-->glycolysis-->lactate
4. lactate to liver
in liver:
5. lactate-->pyruvate-->OAA-->gluconeogenesis-->GLUCOSE

**no G6Pase enzyme

Front 69

eating after fasting - where does glucose go first?

Back 69

glucose taken to muscle first (when BG still low)

hexokinase has lower Km, meaning glucose will go to muscle cells (enters through fac. diffusion)

Front 70

feasting - after all cells have met energy requirements

Back 70

glucose stored as glycogen (mostly in muscle/liver)

1. glucose-->G6P-->UDP-glucose
2. UDP-glucose+glycogen(n)--(glycogen synthase)-->glycogen (n+1)
pos: posphatase, insulin, G6P
neg: kinase, glucagon, glycogen

Front 71

feasting - after glycogen stores are filled

Back 71

FA synthesis (high levels of glucose)

7 malonyl CoA+Acetyl CoA+14 NADPH+H --(FA synthase)--> Palmitate+8 CoA+7 CO2 + 6 H2O + 14NADP

glucose goes to liver when BG is high
glucose high=G6P high=inhibits HK

Front 72

bad idea to supplement w/ individual AAs

Back 72

AA's share common transporters; too much of 1 AA may crowd out others that share that transporter and inhibit absorption

Front 73

why body runs on gluconeogenesis when its starving (even though it costs energy)

Back 73

RBCs can only use glucose, brain prefers glucose, and cell is operating anaerobically

Front 74

2 molecules that can pick up free ammonium ion

Back 74

1. alpha-kg+NH4-->glutamate
2. glutamate+NH4--(glutaminase)-->glutamine

Front 75

molecuse that CARRY nitrogen from trans/deamination rxns

Back 75

transamination - alanine

deamination - glutamine