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Brain and Behavior Exam 3 > Lec 51 Neurobiology of Feeding > Flashcards

Lec 51 Neurobiology of Feeding Flashcards

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1
Q

What is equation of BMI?

A

BMI = weight in KG/(height in m)^2

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2
Q

What are diagnostic criteria for anorexia nervosa?

A
  • body weight 15% or more below normal
  • fear of being fat despite being underweight
  • grossly distorted body image
  • in women often accompanies by amenorrhea
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3
Q

What BM I for overweight? oese?

A

BMI > 25 overweight

BMI > 30 obese

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4
Q

What are health risks associated wtih obesity?

A
  • CV disease
  • diabetes
    some forms of cancer
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5
Q

What hormones are increased in anorexic? decreased?

A

increase: cortisol, growth hormone
decreased: thyroid hormone

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6
Q

What is definition bulimia?

A

alternating periods of bing + purge

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7
Q

What happens to feeding in lesion of lateral hypothalamus?

A

extreme hypophagia, starvation

—> LH contains pro-appetite orexigenic factors

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8
Q

What happens to finding in lesion of medial hypothalamus?

A

hyperphagia and obesity
particularly ventromedial hypothalamus

–> MH contains anti-appetite anorexigenic factors

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9
Q

What is a major brain reward system?

A

mesolimbic dopamine system = DA neurons from ventral tegmental of midbrain to ventral striatum (nucleus accumbens) and limbic cortex

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10
Q

How is mesolimbic dopamine system associated with feeding?

A

mediates desire for food a a primary rewarding substance (appetite)

– particularly fat, salt, sugar

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11
Q

How does hypothalamus control feeding behavior?

A

intragrates need for food via signals from periphery (hunger)

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12
Q

What is role of cerebral cortex in feeding control?

A

exerts control over feeding behavior based on cognitive experiences

may integrate with psych and social factors

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13
Q

How is efficiency of mitochondria tied to body weight?

A

more efficient = use less energy = gain weight

less efficient = use more energy = lose weight

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14
Q

What hormone is the major controller of appetite in the body? Where is it made? where does it act primarily?

A

leptin
synthesized in fat cells –> amount of leptin proportional to volume of fat

act: primarily on hypothalamus

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15
Q

What is action of leptin when you lose weight?

A

losing weight decreases leptin

  • -> get increased orexigenic and decreased anorexigenic factors
  • -> increased food intake, parasympathetic tone, decreased energy use
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16
Q

What is function of leptin?

A

acts in hypothalamus

  • decreases feding
  • increases energy utilized by: increasing activity, increasing thermogenesis (mitochrodrial effect)
  • decreases energy storage (less fat)
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17
Q

What is mech of Ob and Db mice?

A 
Ob = knockout of gene that produces leptin
Db = knockout of gene that encodes for leptin receptor
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18
Q

How does leptin enter brain?

A

transported to hypothalamic region by specific transport protein

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19
Q

What is the leptin receptor?

A

receptor for leptin

activates JAK-STAT pathway

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20
Q

Where does leptin act specifically and what specific peptides does it inhibit/stimulate?

A

acts in arcuate nucleus of hypothalamus to

  • inhibit NPY and AgRP = two orexigenics
  • stimulates aMSH and CART = 2 anorexigenics
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21
Q

Where do leptin’s targets act?

A
  • act on other peptides in hypothalamus that mediate reduction in feeding + increased energy use

–> NPY and AgRP stimulate MCH and inhibit CRF/TRF

–> a-MSH and CART stimulate CRF and inhibit MCH [but luckily aMSH and CART are downregulated by leptin]

  • inhibit MCH in lateral hypothalamus
  • stimulate CRF and TRF in paraventricular nucleus in medial hypothalamus
MCH = melanin-concentrating hormone = orex.
CRF = corticotropin releasing = anorex.
TRF = thyrotropin releasing = anorex.
22
Q

What type of nerve cells make releasing factors in paraventricular nucleus of hypothalamus?

A

parvocellular neurons

23
Q

What else besides MCH exists in lateral hypothalamus that is associated with weight?

A

orexin

24
Q

What is neuropeptide Y (NPY)? where is it synthesized?

A
  • most powerful orexigenic factor known

- synthesized in arcuate nucleus

25
Q

What to NPY knockouts look like?

A

very skinny

26
Q

What is action of NPY?

A

from arcuate nucleus porjects to PVN of hypothalamus to inhibit anorexigenics (CRF) and to lateral hypo to stimulate orexigenics (MCH)

27
Q

What kind of G receptors for orexigenic peptides vs anorexigenics?

A 
orexigenics = Gi linked
anorexigenics = Gs linked
28
Q

What is melanocortin (aMSH)? where is it synthesized?

A
  • derived from POMC peptide that also encodes for ACTH and endorphins
  • synthesized in anterior pituitary and arcuate nucleus of hypo.
  • important anorexigenic
29
Q

What is action of melanocortin?

A
  • acts via MC4 [Gs linked] receptor

- stimulate other anorexigenics in PVN (CRF) and inhibits orexigenics in lateral hypo (MCH)

30
Q

What is mech of action of AgRP?

A

antagonist of aMSH MC4 receptor

31
Q

What do AgRP mice look like?

A

skinny

32
Q

What do MC4 knockout mice look like?

A

obese = late onset oesity

33
Q

What is MCH? where is it expressed?

A

melanin-concentrating hormone?

  • expressed in lateral hypothalamus
  • orexigenic, acts via MCH Gi receptors
34
Q

What do MCH knockout mice look like?

A

skinny

35
Q

Where is AgRP synthesized?

A

arcuate nucleus

36
Q

What are agouti mice?

A
  • develop late-onset obesity

- Agouti acts like AgRP to inhibit a-MSH activation of MC4 receptors

37
Q

What is orexin [hypocretin]? where is it expressed?

A

expressed in lateral hypothalamus

  • pro-feeding [orexigenic]
  • promotes feeding via enhanced wakefulness/arousal
38
Q

What happens if you destroy orexin neurons?

A

get narcolepsy

39
Q

What is ghrelin? action?

A
  • secreted by stomach when you fast
  • orexigenic
  • acts on NPY/AgRP neuron growth receptor
  • may directly act on VTA Da neurons to promote drive for food
40
Q

What is GLP-1? action?

A

glucagon-like peptide-1

  • secreted by intestinal L cells in response to feeding
  • strong anorexigenic
  • acts mainly on GLP1 receptor in periphery to stimulate insulin release, reduce glucagon
  • acts directly on hypothalamus to decrease food intake
41
Q

What is exenatide?

A

GLP-1 agonist

used for treatment type 2 diabetes

42
Q

How does insulin act on brain feeding?

A
  • acts directly to inhibit NPY/AgRP neurons in arcuate nucleus of hypothalamus
  • reduces feeding behavior
43
Q

Is obesity genetic? examples?

A

yes but mech not totally known

  • FTO (fat mass and obesity-associated protein)
44
Q

What are hypothetical treatments for obesity?

A

agonists of anorexigenic factor receptors, antagonists of orexigenic receptors

45
Q

How is dopamine associated with weight control?

A

DA in VTA-NAc path promotes appetitde

regulates drive for food

46
Q

How do amphetamines effect appetite?

A

act by increasing DA rand 5HT elease in hypothalamus

new drug = bupropion/naltrexone

47
Q

What are effect of serotonin function enhancers on appetite?

A
  • fenfluramine, SSRIs, fen-phen enhance serotonin and suppress appetite
    mech unknown
48
Q

What do 5Ht2C receptor knockout mice look like?

A

develop adult obesity
recent release lorcaserin = 5HT2c agonist
may be due to activation of 5HT2C causes activation of melanocortin nueorns –> stimulate release of melanocortin = anorexigenic

49
Q

How are cannabinoids associated with weight control?

A
  • act at CB1 receptor in brain –> stimulate munchies
  • CB1 antagonists as appetite suppresants
    BUT: side effect of depression and suicide
50
Q

Are there leptin abnormalities in anorexia/bulimia?

A
  • nope

- but leptin levels rise excessively with refeeding –> impede recovery

Brain and Behavior Exam 3 (32 decks)

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