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The hypothalamus releases peptides influencing feeding behavior.
Two hypothalamic neuronal groups participate in this process.
Neuropeptide Y (NPY) and Agouti-related peptide (AgRP) neurons in the arcuate nucleus stimulate appetite by releasing neuropeptide Y and Agouti-related peptide.
In contrast, Pro-opiomelanocortin P-O-M-C or Cocaine- and Amphetamine-Regulated Transcript CAR-T neurons suppress appetite by releasing alpha-melanocyte-stimulating hormone and cocaine- and amphetamine-regulated transcript.
Short-term appetite regulation involves neural signals, nutrient levels in the blood, and GI hormones.
These signals stimulate the hypothalamus via the solitary nucleus in the brainstem.
Increased levels of glucose, amino acids, and fatty acids in the blood, and distention of the GI tract signal fullness and suppress hunger.
Further, gut hormones like insulin and cholecystokinin signal satiety to suppress hunger. In contrast, ghrelin, a stomach hormone, stimulates appetite.
Leptin, a hormone produced by adipose cells, suppresses appetite. However, in obesity, leptin resistance renders high leptin levels ineffective, contributing to weight gain.
Short-term regulation of food intake primarily involves neural signals from the gastrointestinal (GI) tract, blood nutrient levels, and GI tract hormo…
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