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Biol 4890 > Chapter 27 > Flashcards

Chapter 27 Flashcards

1
Q

caloric homeostasis

A

adequate but not excessive energy

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2
Q

appetite suppression signals

A

CCk and GLP-1

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3
Q

Appetite Enhancing Signal

A

Ghrelin

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4
Q

CCK mechanism

A

released by intestine into brain . binds g-protein. causes feelings of satiety. releases bile salts.

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5
Q

GLP-1 hormone mechanism

A

released by intestine into pancrease . binds g-protein. causes increased insulin secretion and b-cell proliferation.

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6
Q

long term caloric homeostasis is controlled by ? (2)

A

Leptin and insulin

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7
Q

Leptin Mechanism

A

Leptin is an adipokine released by adipocytes. signals the status of TAG stores.

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8
Q

mice that lack leptin are ?

A

obese

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9
Q

leptic active at high/low AMP concentration

A

high

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10
Q

neurons associated with Leptin pathway

A

NPY, agRP, and POMC

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11
Q

NPY and agRP are appetite stimulants/supressors

A

stimulants

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12
Q

POMC is appetite stimulants/supressors

A

suppressing

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13
Q

SOCS aka

A

supressors of cytokine signalling

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14
Q

SOCS interfere with ? and ?

A

leptin and insulin signalling

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15
Q

obese have high/low leptin levels. implicated to be caused by ?

A

high. SOCS

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16
Q

insulin signalling pathway

A

insulin signals phosphorylation/activation of IRS. Activates P13K. Activates PDK. Activates AKT. Activates GSK-3. Phosphorylates/deactivates glycogen synthase.

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17
Q

activation of glycogen synthase

A

PP1 phosphatase dephosphorylates

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18
Q

diabetes type 2 cause

A

excess TAG in adipose as a result of caloric excess. Causes insulin resistance

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19
Q

basic strategy of catabolism

A

make NADH, ATP and build blocks for biosynthesis

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20
Q

basic strategy of anabolism

A

use NADPH, ATP and building blocks for biosynthesis

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21
Q

Three major pathways that occur in cytoplasm

A

glycolysis, pentose phosphate, fatty acid synthesis

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22
Q

major pathway in mitochondrial inner membrane

A

oxidative phosphorylation

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23
Q

Three major pathways in mitochondrial matrix

A

CAC, b-oxidation of fatty acids, ketone body formation

24
Q

PFK regulation

A

activated by F26BP and AMP. Inhibited by ATP and citrate.

25
Q

fructose 1,6-bisphosphatase

A

activated by citrate. inhibited by AMP and F26BP.

26
Q

Reciprocal control by PFK2

A

phosphorylation of by PKA turns off glycolysis. dephosphorylation makes F26BP turning glycolysis on.

27
Q

pentose phosphate primarily regulated by availability if ?

A

NAD+

28
Q

glycogen phosphorylase and ? are under reciprocal control

A

glycogen synthase

29
Q

major control point in fatty acid synthesis

A

citrate stimulates acetyl CoA carboxylase and provides substrate for commited step

30
Q

fatty acid degradation control point

A

inhibited by fatty acid synthesis

31
Q

four fates of G6P

A

G1P, F6P, 6PG, glucose

32
Q

G6P makes G1P when ? for ?

A

G6P and ATP are high. glycogen synthesis

33
Q

G6P makes F6P when ? for ?

A

ATP or carbon skeletons are needed. Glycolysis.

34
Q

G6P makes 6PG when ? for ?

A

cell needs NADPH or ribonucleotides. pentose phosphate.

35
Q

Brain Energy.

A

Use 60% of bodies glucose in maintaining membrane potential. Ketone bodies replace glucose as fuel during starvation.

36
Q

Kidneys transport 60 volumes of blood driven by cotransport of ? using ?

A

Na+ using Na+/K+ ATPase

37
Q

adipose tissue is specialized for ?

A

esterification of fatty acids to form TAGs and breakdown

38
Q

preferred fuel in resting muscle

A

fatty acids

39
Q

preferred fuel in of muscle in times of high ATP use

A

glucose

40
Q

glycolysis outpaces TCA when large amounts of ATP are needed leading to production of ?

A

lactic acid

41
Q

muscle produces alanine by transamination of ?

A

pyruvate

42
Q

metabolic hub that gets first call on nutrients and distributes fuel to other tissues

A

liver

43
Q

regulates lipid metabolism

A

liver

44
Q

takes up most of the glucose in blood and stores it as glycogen

A

liver

45
Q

well fed state conditions

A

glucose and AA’s transported in blood. insulin released to stimulate energy storage and protein synthesis. glycogen storage in muscle and liver occurs. liver able to trap large amount of glucose because it has a glucokinase with high Km or high affinity for glucose.

46
Q

early fasting state conditions

A

decreased insulin secretion. increased glucagon levels. liver releases glucose to bloodstream. adipose tissues release fatty acids and muscle and liver use fatty acids as fuels

47
Q

adaptations in starvation

A

muscle use fatty acids exclusively. pyruvate dehydrogenase turned off. pyruvate, lactate and alanine sent to liver for gluconeogenesis. gluconeogenesis depeletes TCA intermediates. excess acetyl CoA used to produce ketone bodies. less glucose demand decreases protein breakdown.

48
Q

ketone body sythesis from acetyl CoA

A

(thiolase)> acetoacetyl CoA >(HMG CoA synthase)> HMG-CoA >(HMG CoA Lyase)> acetoacetate

49
Q

type 1 diabetes

A

lack of insuline

50
Q

ATP and creatine-P supply enough ATP for ? seconds of sprinting

A

6

51
Q

slowest method of ATP production

A

utilization of fatty acids

52
Q

as distance running increases, we rely more on aerobic/anaerobic ATP production

A

aerobic

53
Q

Alcohol metabolism

A

ethanol oxidized to acetaldehyde in the cytoplasm and to acetate in mitochondria increasing NADH

54
Q

Alcohol effects on liver metabolism

A

NADH accumulation inhibits gluconeogenesis and fatty acid oxidation. Acetate is converted to acetylCoA which stimulates fatty acid synthesis (b/c NADH inhibits TCA cycle) resulting in “fatty liver”. Ketone body production increases which can lower blood ph. acetate processing eventually impaired and acetaldehyde accumulates causing liver damage.

55
Q

ethanol induced P450 pathway

A

consumes NADPH as it oxidizes ethanol. generates damaging free radicals and reduces ability to generate antioxidant reduced glutathione.

56
Q

scurvy

A

disease from vitC deficiency. insufficient hydroxylation of proline in collagen.

Biol 4890 (16 decks)

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