title: Glucose regulation in non-insulin-dependent diabetes mellitus. Interaction between pancreatic islets and the liver.
abstract: The degree of fasting hyperglycemia in patients with non-insulin-dependent diabetes mellitus is dependent on the rate of hepatic glucose production. The basal rate of hepatic glucose production is increased in patients with non-insulin-dependent diabetes mellitus, and there is a positive correlation between hepatic glucose production and fasting glucose levels. Diminished secretion of insulin, impaired hepatic sensitivity to insulin's effects, or a combination of these factors could contribute to the elevated hepatic glucose production in patients with non-insulin-dependent diabetes mellitus. The relationship between insulin secretion and hepatic glucose production is regulated by a closed feedback loop operating between glucose levels and pancreatic beta cells. Although fasting insulin levels are usually comparable between patients with non-insulin-dependent diabetes mellitus and normal subjects, insulin secretion is markedly impaired in non-insulin-dependent diabetes mellitus in relation to the degree of hyperglycemia present. In fact, the degree of fasting hyperglycemia in a given patient with non-insulin-dependent diabetes mellitus is closely related to the degree of impaired pancreatic beta-cell responsiveness to glucose. Such findings suggest that impaired insulin secretion leads to increased hepatic glucose production, which raises the plasma glucose level. The resulting hyperglycemia helps to maintain relatively normal basal insulin output. Chronic sulfonylurea drug therapy of patients with non-insulin-dependent diabetes mellitus enhances pancreatic islet sensitivity to glucose, leading to increased insulin secretion, suppression of hepatic glucose production, and a decline in the steady-state fasting glucose level.
authors.forename: J B
authors.initials: JB
authors.lastname: Halter
authors.forename: W K
authors.initials: WK
authors.lastname: Ward
authors.forename: D
authors.initials: D
authors.lastname: Porte
authors.forename: J D
authors.initials: JD
authors.lastname: Best
authors.forename: M A
authors.initials: MA
authors.lastname: Pfeifer
mesh_terms: D001120:Arginine; D001786:Blood Glucose / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000503:physiopathology* / Q000628:therapy; D005215:Fasting; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005246:Feedback; D005934:Glucagon / Q000502:physiology; D005943:Gluconeogenesis; D005947:Glucose / Q000096:biosynthesis*; D006003:Glycogen / Q000378:metabolism; D006706:Homeostasis; D006801:Humans; D007328:Insulin / Q000378:metabolism / Q000627:therapeutic use; D007333:Insulin Resistance; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000503:physiopathology*; D008099:Liver / Q000503:physiopathology*; D013004:Somatostatin / Q000502:physiology; D013453:Sulfonylurea Compounds / Q000627:therapeutic use
chemical_list: D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D013453:Sulfonylurea Compounds; D013004:Somatostatin; D006003:Glycogen; D005934:Glucagon; D001120:Arginine; D005947:Glucose