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GIGU Midterm > Regulation of Food Intake > Flashcards

Regulation of Food Intake Flashcards

1
Q

where are the neuronal centers that control feeding and satiety located?

A

within the hypothalamus

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2
Q

how does the hypothalamus receive signals from the GI tract?

A

via the vagus nerve

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3
Q

where does most of the integration signaling regulating food intake and energy expenditure happen?

A

in the arcuate nucleus

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4
Q

what neurons are involved in the anorexigenic pathway?

A

pro-opiomelanocortin (POMC) neurons or CART

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5
Q

what stimulates the POMC/CART neurons?

A

insulin, leptin, and CCK

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6
Q

what happens when insulin, leptin, or CCK stimulate the POMC/CART neurons?

A

they will release alpha-MSH

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7
Q

where does the alpha-MSH bind to in the anorexigenic pathway?

A

on their receptors- MCR-4 on the second order neurons in the paraventricular nucleus

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8
Q

what is the result of alpha-MSH binding to the MCR-4 receptors

A

decreased food intake and an increase in energy expenditure

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9
Q

what neurons are involved in the orexigenic pathway?

A

AGRP and NPY

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10
Q

what stimulates the AGRP and NPY neurons?

A

Ghrelin

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11
Q

what inhibits the AGRP and NPY neurons?

A

insulin, leptin, and CCK

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12
Q

what does NPY bind to?

A

its receptor- Y1R on the second order neuron in the PVN

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13
Q

what is AGRP an antagonist of?

A

MCR-4

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14
Q

what happens when NPY binds to its Y1R receptor on the second order neuron in the PVN?

A

it will result in an increase in food intake

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15
Q

what have some cases of obesity been related to?

A

mutations in the POMC and MCR-4 genes

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16
Q

what is the finding with prader-willi syndrome?

A

partial deletion of chromosome 15

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17
Q

what are the symptoms of prader willi syndrome?

A

small hands and feet, hyperphagia, and paradoxically elevated ghrelin

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18
Q

several peptides that stimulate satiety and decrease feeding activate what?

A

receptors on vagal afferents

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19
Q

where do the vagal afferents travel?

A

to the nucleus tractus solitarius and then to the hypothalamus

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20
Q

what kind of information do the vagal afferents carry?

A

gastric distention, levels of gut hormone, type of lumenal content

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21
Q

what is considered to be the hunger center?

A

the lateral hypothalamic areas (LHA)

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22
Q

what is considered to be the satiety center?

A

the ventromedial hypothalamic nucleus

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23
Q

what is ghrelin secreted by?

A

endocrine cell in the stomach

24
Q

what does ghrelin stimulate?

A

neurons that release NPY

25
Q

what is the only known orexogenic gut hormone?

A

ghrelin

26
Q

what is ghrelin release associated with?

A

increased appetite- it appears to initiate the feeding response

27
Q

where does insulin bind?

A

to receptors in the POMC and NPY systems

28
Q

what happens when insulin binds to the POMC system?

A

it is going to stimulate it

29
Q

what happens when insulin binds to the NPY system?

A

it is going to inhibit it

30
Q

what is the action of insulin?

A

it is going to decrease appetite and increase metabolism

31
Q

what is CCK released by?

A

I cells in the duodenum

32
Q

what does release of CCK do?

A

elicits satiety

33
Q

what is the mechanism of CCK release?

A

it is going to act on the vagus nerve, which then travels to the NTS, and then to the hypothalamus circuit

34
Q

what are the actions of CCK?

A

it is going to cause an inhibition of the release of ghrelin; it is also going to increase gastric distention and therefore decrease gastric emptying

35
Q

what is PYY release by?

A

L cells of the ileum and the colon following a meal

36
Q

what does PYY bind to?

A

Y2R in the hypothalamus

37
Q

what is the action of PYY?

A

it is going to inhibit NPY neurons and it is going to release the inhibition of POMC neurons (so it promotes the anorexigenic pathway)

38
Q

what is leptin secreted by?

A

cells in adipose tissue

39
Q

what does leptin bind to?

A

receptors in POMC and NPY systems

40
Q

what happens when leptin binds to the NPY pathway?

A

it is going to inhibit it

41
Q

what happens when leptin binds to the POMC pathway?

A

it is going to stimulate the POMC pathway

42
Q

what are the actions of leptin?

A

it is an appetite-supressing hormone; it causes decreased appetite, increased metabolism, and decreased ghrelin release

43
Q

obesity in humans is often associated with what type of levels of leptin?

A

high leptin levels and failure to respond to exogenous leptin (leptin resistance)

44
Q

What type of regulation is adiposity signals (leptin) involved in?

A

long-term regulation of energy balance

45
Q

what is glucagon-like peptide co-secreted with?

A

PYY from L cells in the intestin

46
Q

when do the levels of glucagon-like peptide rise and fall?

A

levels rise after a meal and fall during fasting

47
Q

what are the actions of glucagon-like peptide?

A

reduce food intake, suppresses glucagon secretion, and delays gastric emptying

48
Q

where is oxyntomodulin released from?

A

released from L cells of the intestine in response to ingested food

49
Q

what is the effect of oxyntomodulin?

A

anorectic effect

50
Q

where is pancreatic peptide (PP) secreted from?

A

from cells in the pancreatic islets of Langerhans

51
Q

what is the action of pancreatic peptide?

A

it decreases food intake directly through Y4R in the brainstem and the hypothalamus; may also act via the vagus nerve to produce anorectic effects

52
Q

what is the action of glucagon?

A

increase blood glucose levels and insulin secretion and reduces food intake

53
Q

where is amylin stored and released from?

A

stored and released with insulin in response to food intake

54
Q

what is the effect of amylin?

A

anorectic effects (inhibition of NPY release)

55
Q

what is anorexia nervosa characterized by?

A

self-starvation and excessive weight loss

56
Q

what biological factors are related to anorexia nervosa?

A

polymorphisms in genes involved in eating attitudes; basal and pulsatile secretion of leptin is reduced; ghrelin resistance; elevated levels of PYY

GIGU Midterm (19 decks)

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