Regulation of Food Intake Flashcards

(56 cards)

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
what is the only known orexogenic gut hormone?
ghrelin
26
what is ghrelin release associated with?
increased appetite- it appears to initiate the feeding response
27
where does insulin bind?
to receptors in the POMC and NPY systems
28
what happens when insulin binds to the POMC system?
it is going to stimulate it
29
what happens when insulin binds to the NPY system?
it is going to inhibit it
30
what is the action of insulin?
it is going to decrease appetite and increase metabolism
31
what is CCK released by?
I cells in the duodenum
32
what does release of CCK do?
elicits satiety
33
what is the mechanism of CCK release?
it is going to act on the vagus nerve, which then travels to the NTS, and then to the hypothalamus circuit
34
what are the actions of CCK?
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
what is PYY release by?
L cells of the ileum and the colon following a meal
36
what does PYY bind to?
Y2R in the hypothalamus
37
what is the action of PYY?
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
what is leptin secreted by?
cells in adipose tissue
39
what does leptin bind to?
receptors in POMC and NPY systems
40
what happens when leptin binds to the NPY pathway?
it is going to inhibit it
41
what happens when leptin binds to the POMC pathway?
it is going to stimulate the POMC pathway
42
what are the actions of leptin?
it is an appetite-supressing hormone; it causes decreased appetite, increased metabolism, and decreased ghrelin release
43
obesity in humans is often associated with what type of levels of leptin?
high leptin levels and failure to respond to exogenous leptin (leptin resistance)
44
What type of regulation is adiposity signals (leptin) involved in?
long-term regulation of energy balance
45
what is glucagon-like peptide co-secreted with?
PYY from L cells in the intestin
46
when do the levels of glucagon-like peptide rise and fall?
levels rise after a meal and fall during fasting
47
what are the actions of glucagon-like peptide?
reduce food intake, suppresses glucagon secretion, and delays gastric emptying
48
where is oxyntomodulin released from?
released from L cells of the intestine in response to ingested food
49
what is the effect of oxyntomodulin?
anorectic effect
50
where is pancreatic peptide (PP) secreted from?
from cells in the pancreatic islets of Langerhans
51
what is the action of pancreatic peptide?
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
what is the action of glucagon?
increase blood glucose levels and insulin secretion and reduces food intake
53
where is amylin stored and released from?
stored and released with insulin in response to food intake
54
what is the effect of amylin?
anorectic effects (inhibition of NPY release)
55
what is anorexia nervosa characterized by?
self-starvation and excessive weight loss
56
what biological factors are related to anorexia nervosa?
polymorphisms in genes involved in eating attitudes; basal and pulsatile secretion of leptin is reduced; ghrelin resistance; elevated levels of PYY