3 The Genetics of Non-insulin-Dependent Diabetes Mellitus
This chapter discusses the genetics of non-insulin-dependent diabetes mellitus. The chapter provides an overview on the non-insulin-dependent diabetes (NIDDM), which is a genetically heterogeneous disorder of glucose homeostasis and affects approximately 5% of people in Westernized countries. A vari...
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Published in | Advances in Genetics Vol. 32; pp. 51 - 98 |
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Main Authors | , , |
Format | Book Chapter |
Language | English Japanese |
Published |
Elsevier Science & Technology
1995
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Online Access | Get full text |
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Summary: | This chapter discusses the genetics of non-insulin-dependent diabetes mellitus. The chapter provides an overview on the non-insulin-dependent diabetes (NIDDM), which is a genetically heterogeneous disorder of glucose homeostasis and affects approximately 5% of people in Westernized countries. A variety of biochemical abnormalities have been identified in NIDDM, and the relative contribution of these different physiologic or cellular defects differ among patient groups. Acquired factors—such as obesity and a sedentary life style—may be additive, but insulin resistance is considered to be a primary inherited component of the disease. This concept comes from a number of studies, all demonstrating that prediabetic patients are characterized by insulin resistance with normal hepatic glucose metabolism and P-cell function many years prior to the development of NIDDM. Following the transition from the compensated state to frank NIDDM, at least three pathophysiologic changes can be observed. First, there is a marked decrease in P-cell function and insulin secretion. Second, metabolic abnormality occurs in the liver. Patients with impaired glucose tolerance (IGT) have normal basal rates of hepatic glucose production, whereas patients with fasting hyperglycemia have increased rates. Third, metabolic abnormality that occurs following the transition to NIDDM is worsening of the insulin-resistant state. Whether this increment in insulin resistance is secondary to glucose toxicity or other acquired factors remains to be determined. |
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ISBN: | 0120176327 9780120176328 |
ISSN: | 0065-2660 |
DOI: | 10.1016/S0065-2660(08)60203-5 |