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