hypothalamus, obesity and eating Flashcards

1
Q

describe the dual centre model for regulating feeding

A

two parts of the hypothalamus are responsible for two different functions
lateral hypothalmus: feeding centre (lesioned –> emancipated)
ventral medial hypothalamus: satiety centre (lesioned - fat)

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2
Q

describe lipostatic theory

A

that they body and brain interact to maintain a constant body weight via leptin

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3
Q

how is leptin produce

A

by ob gene, expressed in adipocytes

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4
Q

how does leptin relate to fat

A

circulates in bloodstream in proportion to fat mass

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5
Q

effects of leptin?

A
  • -> decreased glucose, hence decreased insulin and bw

- ->increaesd temp and metabolic rate.

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6
Q

what are the anorexigenic nt’s

A

POMC CART

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7
Q

what are the orexigenic nt’s

A

NPY AgRP

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8
Q

where are (an)orexigenic neurons located

A

arcuate nucleus in hypothalamus

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9
Q

what happens when body weight increases?

A

leptin increases.
this stimulates anorexigenic nt’s (POMC CART), which turns off lateral hypothalamus (feeding centre), and turns on PVN pathway (CRH, TRH) –> fat burning.
also food seeking behaviour decreased, increased sympathetic arousal to sites involved in energy expenditure

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10
Q

what happens as body weight decreases?

A

decreased leptin
orexigenic neurons in arcuate nucleus (NPY AgRP) activate lateral hypothalamus (stimulate feeding), turn off PVN pathways
increased feeding behaviour
decreased sympathetic arousal to sties involved in energy expenditure

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11
Q

what are the short term orexigenic signals?

A

ghrelin

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12
Q

what are the short term anorexigenic signals?

A

insulin
leptin
CKK
amylin

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13
Q

describe set point theory

A

weight returns to set point

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14
Q

2 studies relating to set point theory?

A
  1. after weight loss, actual energy expenditure < predicted energy expenditure (trying to get weight back to normal)
    after weight gain, actual energy expenditure > preducted energy expenditure
  2. started for 10 weeks, then placed on normal diet. body weight, hence leptin, CCK, amylin decreased then increased. hunger and ghrelin increased then decreased.
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15
Q

describe hedonistic eating

A

eating is reliant on reward pathways - reward pathways are split into liking and wanting

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16
Q

define liking

A

affective: you enjoy eating something

17
Q

describe liking pathways

A

neurons from brainstem synapse with neurons in nucleus accumbens; brainstem neurons release mu opoids which bind to NA, leading to liking of sweet/high fat foods.

18
Q

define wanting

A

motivational: leads to you actually eating

19
Q

describe wanting pathway

A

dopaminergic neurons extend from ventral tegmental area to basal forebrain.
-lesions result in aphagia, but no change to liking