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Details for phenotype: negative regulation of appetite

EndoNet ID: ENP00091

Name

negative regulation of appetite

General information

This phenotype is not pathologic

Links to other resources

GO
MeSH term 68001069

Phenotype triggers

  • normal activity of melanocortin receptor 3
    in arcuate_nucleus_of_hypothalamus
    • Both alpha-Melanocyte-stimulating hormone (alpha-MSH) and agouti-related protein (AGRP) exert effects on energy balance by signaling through melanocortin receptor 3 and that induced an inhibitory influence on appetite and body weight. Alpha-MSH acts as an agonist to the receptor and suppresses feeding, and AGRP conversely stimulates food intake by antagonizing the alpha-MSH signaling. [1]
  • normal activity of melanocortin-4 receptor
    in paraventricular_nucleus_of_hypothalamus
    • A component of the melanocortin system within the arcuate nucleus of hypothalamus consists of a neuronal population that produces proopiomelanocortin (POMC)-derived peptides, such as alpha-melanocyte stimulating hormone, and cocaine- and amphetamine-regulated transcript (CART) peptides, which promote satiety. [2]
    • In the PVN, the peptides derived from the breakdown of POMC (mainly alpha-MSH)are endogeneous agonists of MC4R. [3]
  • normal activity of melanocortin receptor 3
    in paraventricular_nucleus_of_hypothalamus
    • A component of the melanocortin system within the arcuate nucleus of hypothalamus consists of a neuronal population that produces proopiomelanocortin (POMC)-derived peptides, such as alpha-melanocyte stimulating hormone, and cocaine- and amphetamine-regulated transcript (CART) peptides, which promote satiety. [2]
    • In the PVN, the peptides derived from the breakdown of POMC (mainly alpha-MSH)are endogeneous agonists of MC3R. [3]
  • normal activity of CCK-1
    in hypothalamus
    • Cholecystokinin is released by the gastrointestinal system during meals and induces an anorexigenic response. [4]
    • This physiological pathway is believed to be an essential component of postprandial satiety. [5]
    • CCK activates POMC cells in the nucleus of the solitary tract (NTS), which is located in the brainstem. This effect of peripheral CCK is dependent upon melanocortin signaling, because in the absence of MC4R or by pharmacological inhibition of MC4R in the NTS, the anorexigenic effects of CCK are blocked. [6]
  • normal activity of CCK-2
    in hypothalamus
    • Cholecystokinin is released by the gastrointestinal system during meals and induces an anorexigenic response. [4]
    • This physiological pathway is believed to be an essential component of postprandial satiety. [5]
    • CCK activates POMC cells in the nucleus of the solitary tract (NTS), which is located in the brainstem. This effect of peripheral CCK is dependent upon melanocortin signaling, because in the absence of MC4R or by pharmacological inhibition of MC4R in the NTS, the anorexigenic effects of CCK are blocked. [6]
  • normal activity of NPY2-R
    in arcuate_nucleus_of_hypothalamus
    • The short form of peptide YY (PYY3-36) is cleaved from the long form (PYY1-36) by the enzyme dipeptidyl peptidase IV, and decreases food intake when administered peripherally. [7]
    • The anorectic effect of PYY3-36 requires Y2 receptors because it fails to inhibit food intake in Y2 receptor-knockout mice. PYY3-36 decreased NPY mRNA in the ARC and its direct delivery into the ARC was sufficient to decrease food intake, highlighting the probable importance of NPY cells in the anorectic effect of PYY3-36. [8]
    • The effects of PYY3-36 in decreasing food intake are are due to a combination of various mechanisms involving different brain areas (independent of the melanocortin system. [8]
  • normal activity of melanocortin-4 receptor
    in arcuate_nucleus_of_hypothalamus
    • Both alpha-Melanocyte-stimulating hormone (alpha-MSH) and agouti-related protein (AGRP) exert effects on energy balance by signaling through melanocortin receptor 4 and that induced an inhibitory influence on appetite and body weight. Alpha-MSH acts as an agonist to the receptor and suppresses feeding, and AGRP conversely stimulates food intake by antagonizing the alpha-MSH signaling.g. . [1]
Reference