title: Insulin release in type 2 diabetes mellitus.
abstract: Impaired insulin response is a characteristic feature of Type 2 diabetes. Overt diabetes develops when beta-cells fail to release enough insulin to compensate for decreased insulin sensitivity. However, a subgroup of normal weight patients demonstrates a pronounced beta-cell secretory defect and a normal insulin sensitivity. The molecular basis behind the impaired insulin response in Type 2 diabetes is not clear. Our studies in two animal models of this disease (GK rat and ob/ob mouse) suggest that an impaired glucose metabolism may be a primary defect in the stimulus-secretion coupling in the beta-cells in Type 2 diabetes. In the GK rat, three major alterations in the islet metabolism of glucose have been demonstrated: 1) increased glucose utilization but unchanged glucose oxidation; 2) increased glucose cycling and 3) decreased activity of the glycerol phosphate shuttle. In ob/ob animals we have found an increased rate of glucose cycling. These derangements might result in an incomplete closure of ATP-sensitive K(+)-channels with a decreased insulin response as a consequence.
authors: Department of Endocrinology, Karolinska Hospital, Stockholm, Sweden.
authors: S
authors: S
authors: Efendic
authors: A
authors: A
authors: Khan
authors: C G
authors: CG
authors: Ostenson
mesh_terms: D000818:Animals; D003920:Diabetes Mellitus / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000503:physiopathology*; D004195:Disease Models, Animal; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D051379:Mice; D008820:Mice, Obese; D009765:Obesity; D051381:Rats; D017208:Rats, Wistar
chemical_list: D007328:Insulin