ASP has 85% similarity to the murine form of agouti. As ectopic expression of murine agouti leads to the development of the yellow obese syndrome, this is expected to be consistent in humans. The yellow obese syndrome increases the development of many chronic diseases, including obesity, type II diabetes mellitus and tumorigenesis. ASP has similar pharmacological activation to murine agouti, as melanocortin receptors are inhibited through competitive antagonism. Inhibition of melanocortin by ASP can also be through non-competitive methods, broadening its range of effects. The function of ASP differs to murine agouti. ASP effects the quality of hair pigmentation whereas murine agouti controls the distribution of pigments that determine coat color. ASP has neuroendocrine functions consistent with murine agouti, as it agonizes via AgRP neurons in the hypothalamus and antagonizes MSH at MC4Rs which reduce satiety signals. AgRP acts as an appetite stimulator and increases appetite while decreasing metabolism. Because of these mechanisms, AgRP may be linked to increased body mass and obesity in both humans and mice. Over-expression of AgRP has been linked to obesity in males, while certain polymorphisms of AgRP have been linked to eating disorders like anorexia nervosa. The mechanism underlying hyperinsulinemia in humans is consistent with murine agouti, as insulin secretion is heightened through calcium sensitive signaling in pancreatic beta cells. The mechanism for ASP induced tumorigenesis remains unknown in humans. See also Agouti coloration genetics Agouti-related peptide Genomic imprinting Methylation Epigenetics References Further reading External links Peptides Peptide hormones Mammal genes Melanocortin receptor antagonists