Lecture 20: Regulation of Food Intake Flashcards
What are the feeding/satiety centers in the hypothalamus?
Lateral nucleus Ventromedial nucleus Paraventricular nucleus Dorsomedial nucleus Arcuate nucleus
What pathways are regulated by the arcuate nucleus?
Anorexigenic (satiety pathway)
Orexigenic (hungry pathway)
*antagonize each other
Describe the anorexigenic pathway
Satiety factors: Insulin, Leptin, CCK, stomach distension > POMC neurons release a-MSH > binds to MCR-4 > decrease food intake
Describe the orexigenic pathway
Ghrelin > AGRP/NPY neurons release AGRP and NPY > NPY binds to Y1R, AGRP binds to MCR-4 > increase food intake
What happens if there are mutations in POMC and MCR4?
loss of feelings of satiety > can lead to obesity
Genetic causes of obesity: affected genes
Leptin or leptin receptor gene deficiency
Melanocortin 4 receptor gene mutation
Prader Willi syndrome
Proopiomelanocortin (POMC) deficiency
- leptin gene
- MC4R gene
- partial deletion of chromosome 15 (paternally expressed genes)
- POMC genes
What is the pathway of satiety signals for inducing satiety?
satiety signals > vagus N. (nolose ganglion) > NTS in medulla > Arcuate nucleus in hypothalamus > anorexigenic pathway > satiety
What happens when Vagus N. is blocked?
lose input from satiety signals = can’t figure out if you’re full or not
What are the roles of the other appetite centers in terms of regulating appetite?
Lateral nucleus: hunger center (releases MCH and orexins to stimulate hunger pathway)
Ventromedial nucleus: satiety center
Dorsomedial nucleus & Paraventricular nucleus: take input to the cerebral cortex/brainstem
Ghrelin:
How does it affect appetite and how does it do it?
Ghrelin > GHSR on neurons > release of NPY > increase appetite
Effects: increased appetite, gastric motility, acid secretion, adipogenesis
Insulin:
How does it affect appetite and how does it do it?
Insulin inhibits NPY and stimulates POMC > increase satiety
CCK:
How does it affect appetite and how does it do it?
-increases satiety and metabolism
I cells in duodenum > release CCK > Vagus N. > NTS > arcuate nucleus > decrease Ghrelin, gastric emptying, increase distension
PYY:
How does it affect appetite and how does it do it?
-increases satiety and metabolism
L cells in ileum > PYY > bind to Y2R in hyp > inhibit NPY and stimulate POMC
Leptin:
How does it affect appetite and how does it do it?
What kind of obesity does leptin reduce fat mass in?
-increases satiety and metabolism
Adipose > leptin > inhibit NPY and stimulate POMC
congenital leptin deficiency. regular obesity patients do not respond to exogenous leptin
GLP-1 (glucagon like peptide - 1)
- GLP-1 is an incretin that increases after eating and decreases when fasting
- active after eating - decreases food intake, glucagon secretion and gastric emptying
- L cells > GLP 1 with oxyntomodulin