Tuesday 4 - engeland - hypothalamic control of eating Flashcards
Why do we stop eating (3 general ways:)
gastrically?
nervously?
adipose-ally?
production of satiety factors from the GI tract (hormonal (CCK, polycytokinin))
vagus nerve goes to brainstem
leptin produced by fat acts on arcuate nucleus
summary of pre-absorptive satiety factors.
gastric stretch CAUSES SATIETY
gastric nutrient HAS NO EFFECT
intestinal nutrient CAUSES SATIETY
summary of post-absorptive satiety factors
sensors for glucose and free fatty acids in the liver causes satiety
gastric distention causes increase in activity of this nerve and nucleus
vagus -> goes to solitary nucleus in medulla
causes satiety
cholecystokinin (CCK)
what does it do
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)
Ghrelin
what does it do
makes you hungry
secreted by stomach
increased by fastin
orexigenic means increase in appetite
prader-willi syndrome general
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)
leptin general
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
major nucleus for food intake
arcuate nucleus
medial forebrain bundle function
carries axons up to the brain that is important for motivation
lateral hypothalamic area
lesion causes
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
activation of the lateral hypothalamic area (LHA) causes
release of anabolic neurotransmitter (orexin) and hunger
paraventricular nucleus (PVN)
where
stimulation leads to what
next to third ventricle
stimulation causes decrease in eating:
release of catabolic neurotransmitter in brain (corticotropin relseasing hormone or CRH)
arcuate nucleus
neuron types
things that turn this off/on
output to the LHA and PVN regulates eating and not eating
two types of neurons:
- ones that release neuropeptide Y: project to both PVN and LHA and cause increase in eating
leptin turns npY off
- melanocortin neurons: project to both PVN and LHA and cause decrease in eating
leptin turns melanocortin neurons on
one way leptin causes satiety in the brain
goes to the arcuate nucleus:
turns off neuropeptide Y neurons
turns on melanocortin neurons