Increased Insulin Concentrations in Nondiabetic Offspring of Diabetic Parents
Abstract
Insulin resistance is thought by many to be the primary defect that results in non-insulin-dependent diabetes mellitus (NIDDM). An implication of this theory is that prediabetic persons have higher serum insulin levels than normal subjects. We assessed serum insulin concentrations in a cohort of 1497 nondiabetic Mexican Americans, a population at high risk for NIDDM, according to whether their parents or siblings had diabetes. It was assumed that prediabetic persons would be more likely to have strong family histories of diabetes. We found a stepwise increase in fasting insulin levels in nondiabetics with neither, one, or both parents with diabetes (69.8, 77.8, and 94.6 pmol per liter, respectively; P = 0.002). Similar results were observed for insulin sum (the total of insulin concentrations in the fasting state and at 30, 60, and 120 minutes after a 75-g oral glucose load). The differences in insulin sums according to family history remained statistically significant in analyses of covariance, which controlled for variations in body-mass index, body-fat distribution, and level of blood glucose. Subjects without diabetes who had a diabetic sibling had higher fasting concentrations of insulin than subjects without a diabetic sibling (83.2 vs. 69.6 pmol per liter), but the difference was not statistically significant. We conclude that prediabetic persons, who would be expected to be more numerous in kindreds with progressively stronger family histories of diabetes, have hyperinsulinemia. This supports the insulin-resistance hypothesis.
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Re-examination of data from some other studies of high-risk NGT subjects suggests that conclusions disputing the presence of beta-cell dysfunction are erroneous because no difference in insulin responses existed between groups despite insulin resistance, indicating impaired beta-cell adaptation.
“Thus, re-examination of data from some other studies of high risk subjects with NGT would suggest that the conclusions in those papers disputing the presence of beta-cell dysfunction are erroneous because no difference in the insulin responses existed between groups despite the presence of insulin resistance, indicating impaired beta-cell adaptation [108, 109, 110, 111, 112, 113, 114].”
From The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of type 2 diabetes (2003) · cites this paper as [108]
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- Authors
- Haffner, S. M., Stern, M. P., Hazuda, H. P., Mitchell, B. D., & Patterson, J. K.
- Affiliations
- The University of Texas at San Antonio Health Science Center (US)
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 1988-11-17
- Volume
- 319
- Issue
- 20
- Pages
- 1297-1301
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- OpenAlex
- W2340586419
- Cited by
- 238
- References
- 61
- Citations by year
- 2024: 1 · 2020: 1 · 2017: 1 · 2015: 5 · 2014: 1 · 2013: 4 · 2012: 3
- FWCI
- 10.27
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (HL24799)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Keywords
- hyperinsulinemia, insulin resistance, type 2 diabetes, prediabetes, family history of diabetes, Mexican Americans, fasting insulin, oral glucose tolerance
- MeSH terms
- Adult, Blood Glucose, Body Height, Body Weight, Diabetes Mellitus, Type 2, Female, Hispanic or Latino, Humans, Insulin, Male, Prediabetic State
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