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GIGU > Regulation of Food Intake > Flashcards

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
Q

Describe Ghrelin in feeding behavior

A
  • 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
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26
Q

Describe insulin in feeding behavior

A
  • bind receptors in POMC and NPY systems
  • —–>inhibits NPY, + POMC
  • decreases appetite
  • increases metabolism
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27
Q

Describe insulin effects in Type 1 DM related to food intake

A

increased food intake is associated with decreased insulin in type 1 DM

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28
Q

Describe CCK in feeding behavior

A

Released by I cells in duodenum

  • elicits satiety by acting on vagal-NTS-hypo pathway
  • ———> decreases ghrelin
  • decreases gastric emptying
  • ——->increases gastric distention
29
Q

Describe PYY in feeding behavior

A

Released by L cells of ileum and colon after meal

-binds YR2 in hypothalamus to INHIBIT NPY neurons and + POMC neurons

30
Q

Describe Leptin in feeding behavior

A

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
Q

Injection of what hormone in obese children reduces fat mass, hyperinsulinemia and hyperlipidemia?

A

Leptin

32
Q

Obesity in general is associated with high _____ levels and failure to respond to exogenous ____

A

leptin

–>AKA leptin resistance

33
Q

What is released from pancreatic B cells?

A

Insulin

34
Q

What is the site of action of insulin r/t feeding behavior?

A

hypothalamus

35
Q

What hormone decreases appetite and increases metabolism?

A

insulin

36
Q

What hormone is released from fat cells and endocrine cells of the stomach?

A

leptin

37
Q

What are the sites of action of leptin?

A

Hypothalamus and Vagal Afferents

38
Q

What are the effects of leptin on the hypothalamus?

A

Increase POMC

Decrease NPY and AgRP

39
Q

What decreases appetite and ghrelin release, increases metabolism?

A

leptin

40
Q

What is secreted from I cells of duodenum?

A

CCK

41
Q

What is the site of action of CCK in feeding behavior?

A

Vagal afferents

42
Q

What decreases appetite and gastric emptying?

A

CCK

43
Q

What is secreted from L cells of ileum and colon?

A

PYY

44
Q

What are the sites of action of PYY?

A

Hypothalamus

Stomach

45
Q

What are the effects of PYY on the hypothalamus?

A

decrease NPY and AgRP

Increase POMC

46
Q

What decreases appetite and gastric emptying, increases metabolism?

A

PYY

47
Q

What is secreted from endocrine cells of stomach, hypothalamus, LI and SI?

A

Ghrelin

48
Q

What are the sites of action of ghrelin?

A

Hypothalamus

Vagal afferents

49
Q

What are the effects of ghrelin on the hypothalamus?

A

Increase NPY, AgRP

50
Q

What increases appetite, decreases metabolism and leptin release?

A

Ghrelin

51
Q

What is the difference between fat and gut peptide signal in the modulation of food/energy?

A

Adiposity signals–> long-term regulation of energy balance

Gut peptides–> modulate food intake on meal-by-meal basis

52
Q

What reduces food intake, suppresses glucagon secretion and delays gastric emptying?

A

Glucagon-like peptide 1 (GLP-1)

53
Q

What is co-secreted with PYY from L cells in intestine and is also an incretin?

A

GLP-1

54
Q

How are GLP-1 levels affected by meals and fasting?

A

rise after meal, fall during fasting

–>d/t reduces food intake and inhibits glucagon

55
Q

What is released from L cells of intestine in response to ingested food/caloric intake?

A

Oxyntomodulin

–>anorectic effect

56
Q

What decreases food intake directly through Y4R in brainstem and hypothalamus?

A

Pancreatic peptide

57
Q

Where is pancreatic peptide secreted from?

A

pancreatic islets of Langerhans

58
Q

What can act on the vagus nerce to produce anorectic effects?

A

pancreatic peptide

59
Q

What is stored and released with insulin in response to food intake and inhbits NPY release?

A

Amylin

60
Q

What molecules have anorectic effects?

A

Amylin
Pancreatic Peptide
Oxyntomodulin

61
Q

Define anorexia nervosa

A

self-starvation and excessive weight loss

62
Q

What are some biological factors that support habits of patients with anorexia nervosa?

A
  • 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
Q

What are genetic causes of obesity?

A
  • Leptin receptor gene deficiency
  • MC4R receptor gene mutation
  • Prader Willi syndrome
  • POMC deficiency
64
Q

What causes early-onset SEVERE obesity, hyperphagia, and infertility?

A

Leptin deficiency

65
Q

What causes early-onset SEVER obesity, hyerinsulinemia and is the MOST COMMON cause of genetic obesity

A

MC4R mutation

66
Q

What is the most common known genetic cause of obesity?

A

MC4R gene mutation

food inhibition pathway

67
Q

What leads to severe obesity and MR in children with paradoxically elevated ghrelin?

A

Prader-Willi syndrome

–>partial deletion chromosome 15

68
Q

What is related to obesity, red hair, jaundice and adrenal insufficiency?

A

POMC deficiency

food inhibition pathway

GIGU (37 decks)

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