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Physiology III > Absorptive & Postabsorptive Nutrient Utilization II > Flashcards

Absorptive & Postabsorptive Nutrient Utilization II Flashcards

1
Q

define post-absorptive phase

A

NO current nutrient supply

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2
Q

what happens regarding glc during post-absorptive phase?

A

glc absorption stops
blood glc decreases to stim glucagon and inhibit insulin secretion

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3
Q

during post-absorptive phase, liver switches from glc ___ to glc ___

A

utilization to production

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4
Q

what’s the main brain fuel during post-absorptive phase?

A

glc

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5
Q

decreasing levels of glc will stim ___ secretion from liver

A

glucagon

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6
Q

glucagon stim ___ in the liver

A

glycogenolysis

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7
Q

how long does glycogen depot last?

A

8-12 hours at rest/moderate exercise
30 min at high demand/major exercise

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8
Q

glucagon stim ___ in adipose tissue

A

lipolysis

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9
Q

what do epinephrine and norepinephrine do in adipose tissue during post-absorptive phase?

A

stim lipolysis and FA release through beta-adrenoreceptors

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10
Q

what (from the heart) stim lipolysis during post-absorptive, specifically exercise?

A

natriuretic peptide

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11
Q

what stim lipolysis after and during prolonged exercise?

A

growth hormone
cortisol

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12
Q

how are FA mobilized and released from adipose tissue?

A

hormone sensitive lipase (HSL)

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13
Q

what does hormone sensitive lipase do?

A

activated by norepi and glucagon
helps mobilize FA for release from adipose

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14
Q

what’s used for ketone body and VLDL synthesis?

A

NEFA

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15
Q

NEFA circulates as ____, bound to ___, and packaged in VLDL

A

free FA
bound to albumin

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16
Q

why are there multiple different FA transport mechanisms?

A

albumin can saturate during rapid adipose tissue mobilization
albumin can decrease during long phases of nutrient deficiency
VLDL are independent from AA availability

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17
Q

what does CD36 do regarding FA transport?

A

translocates NEFA into cells

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18
Q

what is CD36?

A

membrane protein found on cell surfaces
fatty acid translocase

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19
Q

___ is translocated during absorptive phase following glc and FA uptake, whereas ___ is translocated during post-absorptive

A

absorptive - GLUT4
post-absorptive - CD36

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20
Q

what does LOW serum insulin do regarding muscles/protein during post-absorptive?

A

diminished aa entry into muscle pool
glc entry declines, net protein degradation and use of aa pool for energy

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21
Q

the insulin/glucagon ratio in the ___ determines action of antagonistic enzyme pairs

A

liver

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22
Q

during post-absorptive phase, glucagon ___ (deactivates) glycogensynthase and phosphofructokinase

A

phsophorylates

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23
Q

during post-absorptive, glucagon ___(activates) fructose-1,6 biphosphate and glycogenphosphorylase

A

phosphorylates

24
Q

after how many hours does the body enter a ketosis state?

A

> /= 24 hours without food

25
Q

during phase of prolonged energy deficiency, all ___ stores have been exhausted and some organs start using ___ for energy

A

glycogen
FA

26
Q

can the brain use FA for energy?

A

NOPE
since too large

27
Q

what does the brain use for fuel during energy deficiency?

A

ketones from liver

28
Q

during prolonged energy deficiency, fuel oxidation shifts from ___ to mainly ___ as the source

A

CHO to lipids

29
Q

does lipolysis increase or decrease during energy deficiency?

A

increases

30
Q

what are the three mechanisms the liver does to make use of NEFA?

A
  1. complete oxidation
  2. esterification to form triglycerides
  3. make ketone bodies
31
Q

increased lipid oxidation will ___ terminal glc oxidation

A

decrease

32
Q

during prolonged energy deficiency, the goal is to ___ aa and glc, and utilize ___

A

preserve
use fat

33
Q

what can the liver produce from glc and aa during absorptive phase?

A

FA

34
Q

what are the two possible pathways of FA once it reaches the liver?

A
  1. produce FA for tissue from glc/aa
  2. consume and channel into krebs cycle or ketogenesis
35
Q

how is it determined which pathway to do for liver FA use?

A
36
Q

during absorptive phase (high insulin), malonylCoA ____ CPT-1

A

suppresses

37
Q

during post-absorptive phase and prolonged energy deficiency, malonylCoA is ___ since glucagon inhibits glycolysis

A

low

38
Q

what’s released from adipose and transported to mitochondria via CPT-1?

A

FA

39
Q

what happens to FA in mitochondria?

A

beta-oxidation and ketone body synthesis

40
Q

describe the normal fat metabolism during prolonged energy deficiency

A
41
Q

what causes hepatic lipidosis in cats?

A
  1. overwhelming hepatocyte capacity (obesity, diabetes), increased NEFA mobilization
  2. damage of hepatozytes, reduction of FA oxidation
  3. protein malnutrition (less apoproteins)
42
Q

list some diseases that are associated with hepatic lipidosis in cats?

A
43
Q

how can you treat hepatic lipidosis>

A

high protein diet

44
Q

how do ruminants maintain glc homeostasis?

A
45
Q

how does glc homeostasis occur during cattle milk production?

A

hgih glc demand for lactose and FA for milk fat
glc -> glycerol
acetate and beta-hydroxybutyrate -> FA
ketones supply energy

46
Q

dairy cows tend to have a ___ energy balance during last 3 weeks before and 6 weeks after parturition. why?

A

negative
since adaption to support lactation

47
Q

which stores are depleted in refeeding syndrome

A

CHO, fat, protein

48
Q

what happens regarding electrolyte balance during refeeding syndrome?

A

not replenished
balance maintained by shift of intracell ions to extracell space, leading to overall depletion
since they will be lost in urine

49
Q

what does refeeding syndrome refer to?

A

complications of refeeding after period of starvation

50
Q

what is the effect of insulin on electrolyte homeostasis?

A

reuptake K

51
Q

what remains in homeostasis during refeeding syndrome?

A

electrolytes
vitamins
extra/intra-cellular fluids

52
Q

in refeeding syndrome, insulin levels ___ and glucagon levels ___

A

insulin - decrease
glucagon - increase

53
Q

what’s the therapy strategy for refeeding syndrome?

A

low CHO, high fat diet
adequate K, PO4, Mg

54
Q

how does metabolism respond immediately and longterm to changes in availability of metabolic fuels?

A
55
Q

which metabolic changes occur during phases of negative energy balance?

A
56
Q

how has the body changed after long phases of nutrient deficiency? (RS)

A

Physiology III (18 decks)

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