Appetite regulatory pathways

Appetite regulatory pathways encompass a complex set of central and peripheral mechanisms that maintain energy homeostasis by integrating signals of energy availability and need. Central regulation occurs mainly in the hypothalamic arcuate nucleus, which contains populations of neurons such as pro-opiomelanocortin (POMC) neurons (inhibit appetite) and neuropeptide Y/agouti-related peptide (NPY/AgRP) neurons (stimulate appetite). These neurons receive input from circulating hormones (leptin, insulin, ghrelin, PYY, GLP-1), neural input (vagus nerve, sensory stimuli), and central neurotransmitter systems (dopamine, serotonin, GABA). The limbic system and brainstem also provide important regulatory signals. Peripheral signals originate from adipose tissue (leptin, adiponectin), gastrointestinal tract (ghrelin, CCK, GLP-1, PYY), and pancreas (insulin). This regulation is disrupted in diseases such as obesity and Prader-Willi syndrome. Therapies targeting these pathways include peptide agonists (like MC4R and GLP-1R agonists), receptor antagonists, and drugs modulating central neurotransmitter signaling[1][2][4][5].

Other names

Appetite regulation pathwaysAppetite regulationAppetite pathwaysFeeding regulatory pathwaysEnergy homeostasis pathways

Agonism or antagonism of peptide hormone receptors (e.g., MC4R agonism); Modulation of neurotransmitter pathways (serotonin, dopamine, GABA); Inhibition/stimulation of signaling cascades (MAPK, PI3K/AKT, mTOR, AMPK); Modulation of gut peptide signaling (GLP-1, PYY, CCK).