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Effects of Type 2 Diabetes on the Regulation of Hepatic Glucose Metabolism
  1. Ananda Basu,
  2. Pankaj Shah,
  3. Michael Nielsen,
  4. Rita Basu,
  5. Robert A. Rizza
  1. From the Department of Endocrinology, Mayo Clinic and Foundation (A.B., P.S., R.B., R.A.R.), Rochester, MN; Department of Surgery, Aarhus University Hospital (M.N), Aarhus, Denmark.
  2. Presented in part at the American Federation for Medical Research-sponsored symposium during Experimental Biology 2004, Washington, DC, April 17-21, 2004.
  3. Address correspondence to: Robert Rizza, Mayo Clinic and Foundation, 5 164 West Joseph, 200 1st Street SW, Rochester, MN 55905; e-mail: rizza.robert{at}mayo.edu.

Abstract

Glucose production is inappropriately increased in people with type 2 diabetes both before and after food ingestion. Excessive postprandial glucose production occurs in the presence of decreased and delayed insulin secretion and lack of suppression of glucagon release. These abnormalities in hormone secretion, coupled with impaired insulin-induced suppression of glucose production and stimulation of splanchnic glucose uptake, likely account in large part for the excessive amounts of glucose that reach the systemic circulation for disposal by peripheral tissues following food ingestion. In contrast, when adequate basal insulin concentrations are present, neither glucagon-induced stimulation of glucose production nor glucose-induced suppression of glucose production differs in diabetic and nondiabetic subjects matched for gender, age, and degree of obesity. However, when insulin secretion is defective, lack of suppression of glucagon can cause substantial hyperglycemia by enhancing rates of glucose production. Therefore, normalization of hepatic glucose metabolism in people with type 2 diabetes mellitus likely will require normalization of insulin and glucagon secretion as well as hepatic insulin action.

Key Words
  • glucose production
  • hepatic insulin action
  • glucagon
  • glucose effectiveness

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