Lecture 20: Regulation of Food Intake Flashcards

1
Q

What are the feeding/satiety centers in the hypothalamus?

A
Lateral nucleus
Ventromedial nucleus
Paraventricular nucleus 
Dorsomedial nucleus
Arcuate nucleus
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2
Q

What pathways are regulated by the arcuate nucleus?

A

Anorexigenic (satiety pathway)
Orexigenic (hungry pathway)

*antagonize each other

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3
Q

Describe the anorexigenic pathway

A

Satiety factors: Insulin, Leptin, CCK, stomach distension > POMC neurons release a-MSH > binds to MCR-4 > decrease food intake

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4
Q

Describe the orexigenic pathway

A

Ghrelin > AGRP/NPY neurons release AGRP and NPY > NPY binds to Y1R, AGRP binds to MCR-4 > increase food intake

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5
Q

What happens if there are mutations in POMC and MCR4?

A

loss of feelings of satiety > can lead to obesity

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6
Q

Genetic causes of obesity: affected genes
Leptin or leptin receptor gene deficiency
Melanocortin 4 receptor gene mutation
Prader Willi syndrome
Proopiomelanocortin (POMC) deficiency

A
  • leptin gene
  • MC4R gene
  • partial deletion of chromosome 15 (paternally expressed genes)
  • POMC genes
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7
Q

What is the pathway of satiety signals for inducing satiety?

A

satiety signals > vagus N. (nolose ganglion) > NTS in medulla > Arcuate nucleus in hypothalamus > anorexigenic pathway > satiety

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8
Q

What happens when Vagus N. is blocked?

A

lose input from satiety signals = can’t figure out if you’re full or not

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9
Q

What are the roles of the other appetite centers in terms of regulating appetite?

A

Lateral nucleus: hunger center (releases MCH and orexins to stimulate hunger pathway)
Ventromedial nucleus: satiety center
Dorsomedial nucleus & Paraventricular nucleus: take input to the cerebral cortex/brainstem

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10
Q

Ghrelin:

How does it affect appetite and how does it do it?

A

Ghrelin > GHSR on neurons > release of NPY > increase appetite

Effects: increased appetite, gastric motility, acid secretion, adipogenesis

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11
Q

Insulin:

How does it affect appetite and how does it do it?

A

Insulin inhibits NPY and stimulates POMC > increase satiety

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12
Q

CCK:

How does it affect appetite and how does it do it?

A

-increases satiety and metabolism

I cells in duodenum > release CCK > Vagus N. > NTS > arcuate nucleus > decrease Ghrelin, gastric emptying, increase distension

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13
Q

PYY:

How does it affect appetite and how does it do it?

A

-increases satiety and metabolism

L cells in ileum > PYY > bind to Y2R in hyp > inhibit NPY and stimulate POMC

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14
Q

Leptin:
How does it affect appetite and how does it do it?

What kind of obesity does leptin reduce fat mass in?

A

-increases satiety and metabolism

Adipose > leptin > inhibit NPY and stimulate POMC

congenital leptin deficiency. regular obesity patients do not respond to exogenous leptin

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15
Q

GLP-1 (glucagon like peptide - 1)

A
  • GLP-1 is an incretin that increases after eating and decreases when fasting
  • active after eating - decreases food intake, glucagon secretion and gastric emptying
  • L cells > GLP 1 with oxyntomodulin
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16
Q

Pancreatic peptide
Glucagon
Amylin

A
  • F Islet cells > PP > decrease food intake
  • a islet cells > decrease food intake
  • B cells > insulin + amylin > NPY inhibition > decrease food intake
17
Q

Anorexia nervosa

A
  • reduced fat mass leads to reduced basal and pulsatile leptin secretion
  • Ghrelin resistance - can’t feel hunger
  • increased PYY - suppresses appetite