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Physiology III > Absorptive & Postabsorptive Nutrient Utilization II > Flashcards

Absorptive & Postabsorptive Nutrient Utilization II Flashcards

(56 cards)

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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

Study These Flashcards
A

phosphorylates

24
Q

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

Study These Flashcards
A

> /= 24 hours without food

25
during phase of prolonged energy deficiency, all ___ stores have been exhausted and some organs start using ___ for energy
glycogen FA
26
can the brain use FA for energy?
NOPE since too large
27
what does the brain use for fuel during energy deficiency?
ketones from liver
28
during prolonged energy deficiency, fuel oxidation shifts from ___ to mainly ___ as the source
CHO to lipids
29
does lipolysis increase or decrease during energy deficiency?
increases
30
what are the three mechanisms the liver does to make use of NEFA?
1. complete oxidation 2. esterification to form triglycerides 3. make ketone bodies
31
increased lipid oxidation will ___ terminal glc oxidation
decrease
32
during prolonged energy deficiency, the goal is to ___ aa and glc, and utilize ___
preserve use fat
33
what can the liver produce from glc and aa during absorptive phase?
FA
34
what are the two possible pathways of FA once it reaches the liver?
1. produce FA for tissue from glc/aa 2. consume and channel into krebs cycle or ketogenesis
35
how is it determined which pathway to do for liver FA use?
36
during absorptive phase (high insulin), malonylCoA ____ CPT-1
suppresses
37
during post-absorptive phase and prolonged energy deficiency, malonylCoA is ___ since glucagon inhibits glycolysis
low
38
what's released from adipose and transported to mitochondria via CPT-1?
FA
39
what happens to FA in mitochondria?
beta-oxidation and ketone body synthesis
40
describe the normal fat metabolism during prolonged energy deficiency
41
what causes hepatic lipidosis in cats?
1. overwhelming hepatocyte capacity (obesity, diabetes), increased NEFA mobilization 2. damage of hepatozytes, reduction of FA oxidation 3. protein malnutrition (less apoproteins)
42
list some diseases that are associated with hepatic lipidosis in cats?
43
how can you treat hepatic lipidosis>
high protein diet
44
how do ruminants maintain glc homeostasis?
45
how does glc homeostasis occur during cattle milk production?
hgih glc demand for lactose and FA for milk fat glc -> glycerol acetate and beta-hydroxybutyrate -> FA ketones supply energy
46
dairy cows tend to have a ___ energy balance during last 3 weeks before and 6 weeks after parturition. why?
negative since adaption to support lactation
47
which stores are depleted in refeeding syndrome
CHO, fat, protein
48
what happens regarding electrolyte balance during refeeding syndrome?
not replenished balance maintained by shift of intracell ions to extracell space, leading to overall depletion since they will be lost in urine
49
what does refeeding syndrome refer to?
complications of refeeding after period of starvation
50
what is the effect of insulin on electrolyte homeostasis?
reuptake K
51
what remains in homeostasis during refeeding syndrome?
electrolytes vitamins extra/intra-cellular fluids
52
in refeeding syndrome, insulin levels ___ and glucagon levels ___
insulin - decrease glucagon - increase
53
what's the therapy strategy for refeeding syndrome?
low CHO, high fat diet adequate K, PO4, Mg
54
how does metabolism respond immediately and longterm to changes in availability of metabolic fuels?
55
which metabolic changes occur during phases of negative energy balance?
56
how has the body changed after long phases of nutrient deficiency? (RS)

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