Mechanisms of insulin resistance in non-insulin-dependent (type II) diabetes.

Abstract

Characteristic of both obesity and non-insulin-dependent diabetes mellitus, insulin resistance is triggered at the level of the target tissue and can be induced by three general categories of causes: (1) an abnormal beta cell secretory product, (2) circulating insulin antagonists, or (3) a target tissue defect in insulin action. Decreased numbers of insulin receptors and a post-receptor defect in insulin action both play relative roles in insulin resistance. A general trend, however, indicates that as insulin resistance increases, the post-receptor defect becomes more prominent. Impaired glucose uptake and subsequent increased hepatic glucose oxidation in non-insulin-dependent diabetes mellitus are major contributing factors to fasting hyperglycemia.

• Authors: J M Olefsky, T P Ciaraldi, O G Kolterman
• Journal: The American journal of medicine (Am J Med) Vol. 79 Issue 3B Pg. 12-22 (Sep 20 1985) ISSN: 0002-9343 [Print] United States
• PMID: 3901744 (Publication Type: Journal Article)

Chemical References

• Autoantibodies
• Fatty Acids, Nonesterified
• Insulin
• Insulin Antagonists
• Receptor, Insulin
• Glucose

Topics

• Autoantibodies (immunology)
• Diabetes Mellitus, Type 2 (metabolism)
• Dose-Response Relationship, Drug
• Fasting
• Fatty Acids, Nonesterified (pharmacology)
• Glucose (biosynthesis)
• Glucose Tolerance Test
• Humans
• Insulin (immunology, metabolism)
• Insulin Antagonists (pharmacology)
• Insulin Resistance
• Insulin Secretion
• Islets of Langerhans (metabolism)
• Liver (metabolism)
• Mutation
• Obesity (metabolism)
• Receptor, Insulin (immunology)