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

A

decreases

21
Q

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

A

increased

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
Q

increased TCA cycle

A

generates NADH and FADH2 which are required for and drive ETC

26
Q

increased ETC

A

generates ETC and FAD which are required for and drive TCA

27
Q

increased ADP

A
  • stimulates isocitrate dehydrogenase in TCA

- stimulates ETC to form NAD and FAD

28
Q

isocitrate dehydrogenase

A

isocitate -> alphaketo-gluterate

rate limiting enzyme

29
Q

ETC utilizes NADH

A

decrease in NADH stimulates:
-isocitrate dehydrogenase
-malate dehydrogenase
(NADH inhibits these)

30
Q

decreases O2

A

halts ETC -> increases NADH > inhibits TCA cycle

31
Q

increased Ca

A

stimulates:

  • isocitrate dehydrogenase
  • alpha-ketoglutarate dehydrogenase
32
Q

alpha-ketogluterate dehydrogenase

A

alpha-ketogluterate -> succinyl CoA

33
Q

malate dehydrogenase

A

malate -> oxaloacetate

34
Q

when NADH/NAH ratio increases

A

build up of citrate -> inhibits Acetyl CoA entering TCA and NAD begins to build up again

35
Q

changes that occur with exercise over time

A

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
Q

starvation

A

glucagon and epi markedly increased -> glycogenolysis and lipolysis

37
Q

amenorrhea

A

when body fat <22% of body weight

due to decreased LH and FSH production

38
Q

symptoms of vit deficiency

A

non-specific
fatigue, nausea, loss of appetite
mm pain d/t glycolysis as primary energy source b/c lacking co-enzymes for metabolism

39
Q

riboflavin

A

precursor for FAD and FMN needed for ETC

widely distributed in foods turn over slow, onset slow

40
Q

niacin

A

vit precursor for NAD

can be synthesized from tryptophan so deficiency rare

41
Q

thiamine

A

required for alpha-ketodehydrogenase of TCA

42
Q

pantothenate

A

precursor for CoA

widely distributed in foods

43
Q

Fe deficiency and ETC

A

need non-heme Fe for ETC

decrease in Fe-sulfur center -> lose gradient for e transport