Status
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Details for phenotype: obesity

EndoNet ID: ENP00136

Name

obesity

General information

This phenotype is not pathologic

Links to other resources

OMIM 601665
Medline Plus 003101
Disease database 9099

Phenotype triggers

  • more activity (high ligand concentration, overexpression) of TNFR1
    in adipose_tissue
    • TNF-alpha can act directly on adipocytes to regulate the release of a preformed pool of leptin. Elevated adipose tissue expression of TNF-alpha that occurs in obesity may contribute to obesity-related hyperleptinemia. [1]
    • Leptin secretion is regulatd by TNF-alpha posttranslationally. This secretagogue-like activity is consistent with the existence of regulatable pools of leptin and may contribute in part to the insulin resistance properties of TNF-alpha as well as the adipostatic mechanisms of leptin. [1]
  • more activity (high ligand concentration, overexpression) of leptin receptor
    in adipose_tissue
    • Elevated Leptin expression and increased pasma leptin levels are associated with obesity and are presumably part of an adipostat mechanism [1]
  • melanocortin receptor 3
    in paraventricular_nucleus_of_hypothalamus
    • Dominant mutations in the agouti peptide were known to cause an obese phenotype in mice and this has been proved to be due to the antagonism of melanocortin receptors located in the PVN [2]
  • melanocortin-4 receptor
    in paraventricular_nucleus_of_hypothalamus
    • Dominant mutations in the agouti peptide were known to cause an obese phenotype in mice and this has been proved to be due to the antagonism of melanocortin receptors located in the PVN [2]
Reference