Regulation of Food Intake Flashcards

1
Q

What are neuronal centers that conttrol feeding and satiety?

A
  • lateral nucleus
  • ventromedial nucleus
  • paraventricular nucleus
  • dorsomedial nucleus
  • arcuate nucleus
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2
Q

Where are the centers that control feeding and satiety located?

A

hypothalamus

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3
Q

What is key to maintaining energy balance?

A

cross-talk between neural and hormonal regulation via hypothalamus

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4
Q

What signals converge in hypothalamus?

A

neural from GI tract

chemical from nutrients in blood

GI hormones

adipose tissue

cerebral cortex (small, taste, sight)

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5
Q

Where is most of the integration of signaling that regulates food intake and energy expenditure?

A

arcuate nucleus of hypothalamus

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6
Q

What is the anorexigenic pathway of the arcuate nucleus?

A

first part of arcuate nucleus pathway

–> alpha-melanocortin (a-MSH) released by POMC neurons

–> bind to MCR-4 present in second order neurons

*****DECREASE food intake

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7
Q

What is the orexigenic pathway of the arcuate nucleus?

A

second part of arcuate nucleus pathway

–> neuropeptide Y (NPY) stimulated by hunger signals

–> bind Y1R

–> AGRP released which is an antagonist of MCR-4

**INCREASE food intake

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8
Q

What is related to mutations in POMC and MCR-4 genes?

A

some cases of obesity

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9
Q

Do the arcuate nucleus pathways antagonize each other?

A

Yes–> what activates one inhibits the other

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10
Q

Describe the appetite-inhibiting pathway

A

POMC (appetite-inhibiting neurons) release a-MSH–> bind MC4 receptors on second-order neurons to inhibit food intake and increase metabolism

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11
Q

Describe the appetite-stimulating pathway

A

hunger signals stimulate release of neuropeptide Y–> bind Y1 receptors to increase feeding behavior and storage of calories

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12
Q

What is an antagonist of the MC4 receptor?

A

AgRP released by NPY

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13
Q

Peptides that stimulate satiety and decrease feeding activate receptors on?

A

Vagal afferents

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14
Q

What circuit produces responses related to feeding behavior and metabolism?

A

Vagus–>NTS–>hypothalamus

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15
Q

When does the amount of material in the stomach no longer influence meal size?

A

when vagal activity is blocked

–>also eliminates effects of satiety hormones

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16
Q

What is crucial in interpretation and relaying of peripheral signals from vagus N?

A

NTS

–> nucleus tractus solitarius

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17
Q

What percent of vagal fibers are afferent?

A

75%

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18
Q

What is the purpose of the vagal–>NTS–>hypothalamus pathway?

A

alter feeding behavior and metabolic responses

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19
Q

What is able to regulate food intake in response to peripheral signals even in absence of higher brain center input?

A

NTS (hindbrain)

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20
Q

What nucleus contains neurons that project to cerebral cortex and areas of brainstem?

A

PVN

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21
Q

What is the hunger center?

A

Lateral hypothalamic area

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22
Q

What peptides do the lateral hypothalamic neurons release?

A

orexigenic peptides

–> MCH, orexins A and B

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23
Q

What is the satiety center?

A

ventromedial hypothalamic nucleus

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24
Q

Hormones released from what areas regulate feeding behavior?

A

GI tract
Pancreas
Adipose tissue

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25
Describe Ghrelin in feeding behavior
- secreted in stomach, bind to growth hormone secretagogue receptors - stimulate neurons that release NPY - increase appetite, gastric motility and acid secretion, adipogenesis - decrease insulin secreition - initiates feeding response
26
Describe insulin in feeding behavior
- bind receptors in POMC and NPY systems - ----->inhibits NPY, + POMC - decreases appetite - increases metabolism
27
Describe insulin effects in Type 1 DM related to food intake
increased food intake is associated with decreased insulin in type 1 DM
28
Describe CCK in feeding behavior
Released by I cells in duodenum - elicits satiety by acting on vagal-NTS-hypo pathway - ---------> decreases ghrelin - decreases gastric emptying - ------->increases gastric distention
29
Describe PYY in feeding behavior
Released by L cells of ileum and colon after meal -binds YR2 in hypothalamus to INHIBIT NPY neurons and + POMC neurons
30
Describe Leptin in feeding behavior
Secreted by adipose tissue - bind receptors on POMC and NPY systems - ------> inhibits NPY - -----> + POMC * *Appetite-suppressing hormone - ---------> decreases appetite and ghrelin release - -------> increases metabolism
31
Injection of what hormone in obese children reduces fat mass, hyperinsulinemia and hyperlipidemia?
Leptin
32
Obesity in general is associated with high _____ levels and failure to respond to exogenous ____
leptin -->AKA leptin resistance
33
What is released from pancreatic B cells?
Insulin
34
What is the site of action of insulin r/t feeding behavior?
hypothalamus
35
What hormone decreases appetite and increases metabolism?
insulin
36
What hormone is released from fat cells and endocrine cells of the stomach?
leptin
37
What are the sites of action of leptin?
Hypothalamus and Vagal Afferents
38
What are the effects of leptin on the hypothalamus?
Increase POMC Decrease NPY and AgRP
39
What decreases appetite and ghrelin release, increases metabolism?
leptin
40
What is secreted from I cells of duodenum?
CCK
41
What is the site of action of CCK in feeding behavior?
Vagal afferents
42
What decreases appetite and gastric emptying?
CCK
43
What is secreted from L cells of ileum and colon?
PYY
44
What are the sites of action of PYY?
Hypothalamus | Stomach
45
What are the effects of PYY on the hypothalamus?
decrease NPY and AgRP Increase POMC
46
What decreases appetite and gastric emptying, increases metabolism?
PYY
47
What is secreted from endocrine cells of stomach, hypothalamus, LI and SI?
Ghrelin
48
What are the sites of action of ghrelin?
Hypothalamus | Vagal afferents
49
What are the effects of ghrelin on the hypothalamus?
Increase NPY, AgRP
50
What increases appetite, decreases metabolism and leptin release?
Ghrelin
51
What is the difference between fat and gut peptide signal in the modulation of food/energy?
Adiposity signals--> long-term regulation of energy balance Gut peptides--> modulate food intake on meal-by-meal basis
52
What reduces food intake, suppresses glucagon secretion and delays gastric emptying?
Glucagon-like peptide 1 (GLP-1)
53
What is co-secreted with PYY from L cells in intestine and is also an incretin?
GLP-1
54
How are GLP-1 levels affected by meals and fasting?
rise after meal, fall during fasting -->d/t reduces food intake and inhibits glucagon
55
What is released from L cells of intestine in response to ingested food/caloric intake?
Oxyntomodulin -->anorectic effect
56
What decreases food intake directly through Y4R in brainstem and hypothalamus?
Pancreatic peptide
57
Where is pancreatic peptide secreted from?
pancreatic islets of Langerhans
58
What can act on the vagus nerce to produce anorectic effects?
pancreatic peptide
59
What is stored and released with insulin in response to food intake and inhbits NPY release?
Amylin
60
What molecules have anorectic effects?
Amylin Pancreatic Peptide Oxyntomodulin
61
Define anorexia nervosa
self-starvation and excessive weight loss
62
What are some biological factors that support habits of patients with anorexia nervosa?
- morphs in genes involved in eating attitudes and behavior - secretion of leptin reduced - ghrelin resistance - elevated levels of PYY (contributes to decreased nutrient intake)
63
What are genetic causes of obesity?
- Leptin receptor gene deficiency - MC4R receptor gene mutation - Prader Willi syndrome - POMC deficiency
64
What causes early-onset SEVERE obesity, hyperphagia, and infertility?
Leptin deficiency
65
What causes early-onset SEVER obesity, hyerinsulinemia and is the MOST COMMON cause of genetic obesity
MC4R mutation
66
What is the most common known genetic cause of obesity?
MC4R gene mutation food inhibition pathway
67
What leads to severe obesity and MR in children with paradoxically elevated ghrelin?
Prader-Willi syndrome -->partial deletion chromosome 15
68
What is related to obesity, red hair, jaundice and adrenal insufficiency?
POMC deficiency food inhibition pathway