ABSTRACT
Animals that deposit excessive amounts of body fat and become obese as result of inheritance of single Mendelian genes for obesity have been known since 1905, when Cuenot first described the yellow obese mouse. White adipose tissue is site of lipid storage by the organism, and it is the tissue that can expand to an extraordinary extent during the course of the development of obesity. Adipsin is a differentiation-dependent serine protease which is an abundant secreted protein of fat tissue. The insulin-resistant stage observed in obese-derived skeletal muscle is characterized by an impaired insulin-stimulated glucose uptake. In obese-derived muscles, alterations in insulin action have been attributed to defects in insulin binding, to autophosphorylation of insulin receptor tyrosine kinase, and/or to insulin receptor tyrosine kinase activity. Among the candidates for a peripheral mechanism responsible for onset of obesity is the endocrine pancreas, which displays abnormalities in most animal models of obesity, all of which are hyperinsulinemic and some frankly diabetic.
