Tuesday 4 - engeland - hypothalamic control of eating Flashcards

1
Q

Why do we stop eating (3 general ways:)

gastrically?
nervously?
adipose-ally?

A

production of satiety factors from the GI tract (hormonal (CCK, polycytokinin))

vagus nerve goes to brainstem

leptin produced by fat acts on arcuate nucleus

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2
Q

summary of pre-absorptive satiety factors.

A

gastric stretch CAUSES SATIETY
gastric nutrient HAS NO EFFECT
intestinal nutrient CAUSES SATIETY

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3
Q

summary of post-absorptive satiety factors

A

sensors for glucose and free fatty acids in the liver causes satiety

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4
Q

gastric distention causes increase in activity of this nerve and nucleus

A

vagus -> goes to solitary nucleus in medulla

causes satiety

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5
Q

cholecystokinin (CCK)

what does it do

A

released from duodenum

increases duodenom and gall bladder contraction

releases bile

pyloric constriction, gastric contraction (increase in stomach activity)

CCK receptors on vagal afferents (these are the same mechanoreceptors that are responding to stretch)

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6
Q

Ghrelin

what does it do

A

makes you hungry

secreted by stomach

increased by fastin

orexigenic means increase in appetite

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7
Q

prader-willi syndrome general

A

fetal hypotonia (decreased muscle)

mental retardation

hypogonadotropic hypogonadism (FSH and LH decreased, small testicles in males)

obesity

hyperphagia (means excessive eating)

caused by hyper-ghrelinemia (we think)

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8
Q

leptin general

A

released by adipocytes

causes decrease in food intake

people who are overweight have high amounts of leptin, people who are obese may have less leptin receptor activity

sites of action: brainstem in solitary nucleus, not involved with vagus nerve

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9
Q

major nucleus for food intake

A

arcuate nucleus

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10
Q

medial forebrain bundle function

A

carries axons up to the brain that is important for motivation

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11
Q

lateral hypothalamic area

lesion causes

A

leasion causes aphasia (no eating)

once thought to be just:

may be damage to medial forebrain bundle (causes decreased motivation to eat)

may be due to reduced motor function because your little mouse self cannot get to the food

now we know that it is the loss of neurons that synth orexigenic peptides called orexins

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12
Q

activation of the lateral hypothalamic area (LHA) causes

A

release of anabolic neurotransmitter (orexin) and hunger

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13
Q

paraventricular nucleus (PVN)

where
stimulation leads to what

A

next to third ventricle

stimulation causes decrease in eating:

release of catabolic neurotransmitter in brain (corticotropin relseasing hormone or CRH)

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14
Q

arcuate nucleus

neuron types

things that turn this off/on

A

output to the LHA and PVN regulates eating and not eating

two types of neurons:

  1. ones that release neuropeptide Y: project to both PVN and LHA and cause increase in eating

leptin turns npY off

  1. melanocortin neurons: project to both PVN and LHA and cause decrease in eating

leptin turns melanocortin neurons on

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15
Q

one way leptin causes satiety in the brain

A

goes to the arcuate nucleus:

turns off neuropeptide Y neurons

turns on melanocortin neurons

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16
Q

what does ghrelin do in the brain

A

increases food intake

in the arcuate neurons:

increases npY activity

decreases melanocortin activity?