Biochem review Flashcards

1
Q

liver fnxs

A

maintain blood glucose
synthesize ketones form Acetyl-CoA during lipolysis
synthesize FAs and converts to TGLs and release as VLDLs

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2
Q

requirements for liver fnx

A

absorptive state: glucose and AA for energy

post-absorptive state: lactate, glycerol, and AA for gluconeogenesis

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3
Q

adipose fnxs

A

take up FAs and convert to TGLs for storage

release FAs into circulation

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4
Q

requirements for adipose fnx

A

glucose to produce glycerol phosphate for esterification of FAs
switch to FAs during post-absorptive state

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5
Q

resting skeletal mm fnxs

A

release AAs into blood

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6
Q

requirements for resting skeletal mm fnx

A

absorptive state: glucose for oxidation and glycogen stores, AAs for protein synthesis
post-absorptive state: FAs and ketones for energy

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7
Q

active skeletal mm fnx

A

fast-twitch: anaerobic glycolysis from mm glycogen (primary source of energy)
slow-twitch: oxidative metabolism of glycogen
after several hrs switch to lipolysis

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8
Q

immediate changes after meal

A

BG increases followed by increase in TGs and AAs

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9
Q

increased BG detected by what

A

pancreas -> releases insulin

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10
Q

insulin effects on liver and mm

A

glycogen synthesis increases until maxed then FA production increases
protein synthesis increases in mm

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11
Q

insulin effects on adipose

A

TGs synthesis

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12
Q

insulin effects on brain and red cells

A

nothing

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13
Q

what occurs in post-absorptive/fasting state?

A

glucagon released

epi increases

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14
Q

glucagon on liver

A

glycogenolysis
glucose released in blood
AA and FAs into liver for gluconeogenesis

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15
Q

epi on mm

A

AA released into blood

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16
Q

epi on adipose

A

FAs released into blood

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17
Q

how does mm contraction activate TCA cycle?

A

increased Ca
increased ADP
decrease in NADH/NAD ratio

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18
Q

does NADH dehydrogenase activity increase or decrease in exercise

A

increase b/c using NADH in ETC

19
Q

what happens to lactate dehydrogenase in exercise

A

increases bc converting pyruvate -> lactate

20
Q

what happens to the ATP:ADP ratio in exercise

21
Q

what happens to NADH:NAD ration in intense anaerobic exercise?

22
Q

anaerobic mm metabolism

A

high intensity exercise
ATP need > mito capacity for ox phos
increased lactate production (increased NADH:NAD ratio directs pyruvate-> lactate)
Increased H productin (lactic acid dissociates -> decreased pH -> pain and fatigue)

23
Q

aerobic metabolism

A

low intensity exercise
rate of ATP utilization lower and ox phos sufficent
increased CO2

24
Q

how does exercise increase ATP utilization

A

increased TCA cycle

increased ETC

25
increased TCA cycle
generates NADH and FADH2 which are required for and drive ETC
26
increased ETC
generates ETC and FAD which are required for and drive TCA
27
increased ADP
- stimulates isocitrate dehydrogenase in TCA | - stimulates ETC to form NAD and FAD
28
isocitrate dehydrogenase
isocitate -> alphaketo-gluterate | rate limiting enzyme
29
ETC utilizes NADH
decrease in NADH stimulates: -isocitrate dehydrogenase -malate dehydrogenase (NADH inhibits these)
30
decreases O2
halts ETC -> increases NADH > inhibits TCA cycle
31
increased Ca
stimulates: - isocitrate dehydrogenase - alpha-ketoglutarate dehydrogenase
32
alpha-ketogluterate dehydrogenase
alpha-ketogluterate -> succinyl CoA
33
malate dehydrogenase
malate -> oxaloacetate
34
when NADH/NAH ratio increases
build up of citrate -> inhibits Acetyl CoA entering TCA and NAD begins to build up again
35
changes that occur with exercise over time
increased number of TCA cycle enzymes and decreased lactate production from pyruvate increased number of ETC components increased mito increased vasodilatory capactiy and increased lymph drainage
36
starvation
glucagon and epi markedly increased -> glycogenolysis and lipolysis
37
amenorrhea
when body fat <22% of body weight | due to decreased LH and FSH production
38
symptoms of vit deficiency
non-specific fatigue, nausea, loss of appetite mm pain d/t glycolysis as primary energy source b/c lacking co-enzymes for metabolism
39
riboflavin
precursor for FAD and FMN needed for ETC | widely distributed in foods turn over slow, onset slow
40
niacin
vit precursor for NAD | can be synthesized from tryptophan so deficiency rare
41
thiamine
required for alpha-ketodehydrogenase of TCA
42
pantothenate
precursor for CoA | widely distributed in foods
43
Fe deficiency and ETC
need non-heme Fe for ETC | decrease in Fe-sulfur center -> lose gradient for e transport