Flashcards in GI Appetite Hormones Deck (34):
1
hypothalamus eating centers
feeding center (lat): stim appetite
satiety center (ven): decrease appetite
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Appetite hormones
ghrelin (up)
CCK (down)
glucagon-like peptide (GLP-1) (down)
peptide YY3-36 (PYY3-36) (down)
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ghrelin made by
cells in stomach, SI, hypothalamus
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ghrelin release stimulated by
goes up: before meals
goes down: after eating (esp protein). carbs are temporary.
5
ghrelin levels in obese/anorexic
decrease is absent or blunted w/ obesity
anorexics have chronically high ghrelin - ignore it
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CCK made by
cells in duodenum and jejunum
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CCK release stimulated by
respond to stretch/distension in GI nerves
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CCK effect on brain
short-lived satiety
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ghrelin effect on brain
increase appetite
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GLP-1 made by
ileal L cells
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GLP-1 stimulated by
nutrients in lumen of SI
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GLP-1 actions
stim glucose dependent insulin secretion
suppress glucagon secretion
inhibit gastric secretion (delays absorption of carbs - makes you feel satiated)
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PYY3-36 made by
L cells in SI/LI
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PYY3-36 stim by
after meals
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PYY3-36 actions
bind to NPY receptor (inhibit NPY secretion)
reduce appetite
inhibit gastric motility
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NPY actions
up food intake
up fat storage
reduce anxiety/stress
reduce pain perception
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NPY levels/times
high before meal and high as long as food is w/held
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NPY stimulated by
low: leptin, insulin, PYY
high: ghrelin
(like it is while fasting)
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agouti-related peptide (AgRP)
antagonist of alpha-MSH
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agouti-related peptide actions
increase appetite
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orexigenic factors
increase food consumption
NPY
AgRP
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anorexigenic factors
decrease food consumption
leptin
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leptin stimulated by
levels proportional to body fat
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leptin actions
act on hypothalamus receptors
inhibit appetite (long-term)
"starvation signal" to maintain adequate fat
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absence of leptin -->
uncontrolled food intake and obesity
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leptin resistance mech
usually: feast --> up leptin --> down appetite
fattys: feast all the time --> up leptin --> down regulare receptors --> less regulation of appetite
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insulin and leptin
insulin is leptin-antagonist
chronically high insulin blocks leptin signaling
why? @ puberty/pregnancy need to gain weight - hyperinsulinemic states
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chronic cortisol levels
up food intake
down leptin
up ghrelin
+ makes you store fat in belly
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endocannabinoid (EC) comes from
PHL in cell membranes
(esp omega-6 FAs)
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EC actions
bind to CB-1 receptors -->
brain: stim caloric intake
liver, AT, skeletal muscle, GI: form and store lipids
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EC and obesity
if EC system is overactivated --> weight gain, lipogenesis
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blocking CB-1
EC's cant bind
down food consumption
up weight loss
down body fat
problem: suicidal tendencies
33
satiety vs continuing a meal
satiety signals make GABA released from pre-synaptic neurons to inhibit postsynaptic neuron from continuing the meal
blocked by palatable food, pleasing social, etc --> Ca up --> up EC (bind to CB1 on pre-synaptic) --> down GABA --> keep eating
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