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Research Article Free access | 10.1172/JCI716

Defects in insulin secretion and insulin action in non-insulin-dependent diabetes mellitus are inherited. Metabolic studies on offspring of diabetic probands.

I Vauhkonen, L Niskanen, E Vanninen, S Kainulainen, M Uusitupa, and M Laakso

Department of Medicine, Kuopio University Hospital and University of Kuopio, FIN-70210 Kuopio, Finland.

Find articles by Vauhkonen, I. in: PubMed | Google Scholar

Department of Medicine, Kuopio University Hospital and University of Kuopio, FIN-70210 Kuopio, Finland.

Find articles by Niskanen, L. in: PubMed | Google Scholar

Department of Medicine, Kuopio University Hospital and University of Kuopio, FIN-70210 Kuopio, Finland.

Find articles by Vanninen, E. in: PubMed | Google Scholar

Department of Medicine, Kuopio University Hospital and University of Kuopio, FIN-70210 Kuopio, Finland.

Find articles by Kainulainen, S. in: PubMed | Google Scholar

Department of Medicine, Kuopio University Hospital and University of Kuopio, FIN-70210 Kuopio, Finland.

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Department of Medicine, Kuopio University Hospital and University of Kuopio, FIN-70210 Kuopio, Finland.

Find articles by Laakso, M. in: PubMed | Google Scholar

Published January 1, 1998 - More info

Published in Volume 101, Issue 1 on January 1, 1998
J Clin Invest. 1998;101(1):86–96. https://doi.org/10.1172/JCI716.
© 1998 The American Society for Clinical Investigation
Published January 1, 1998 - Version history
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Abstract

No studies are available that have compared early defects in glucose metabolism in the offspring of insulin-deficient and insulin-resistant probands with non-insulin-dependent diabetes mellitus (NIDDM). To investigate this issue, we evaluated insulin secretion capacity with oral and intravenous glucose tolerance tests and with the hyperglycemic clamp, and insulin action with the euglycemic insulin clamp in 20 offspring of NIDDM patients with low fasting C-peptide (+/-450 pmol/liter), reflecting deficient insulin secretion (IS-group), 18 offspring of NIDDM patients with high fasting C-peptide (>/= 880 pmol/liter), reflecting insulin resistance (IR-group), and 14 healthy control subjects without a family history of NIDDM. The frequency of impaired glucose tolerance was 45.0% in the IS-group and 50% in the IR-group. The IS-group had lower insulin-glucose response at 30 min in the oral glucose tolerance test (85.2+/-10.0 pmol insulin per mmol glucose) than the control group (136.4+/-23.1 pmol insulin per mmol glucose; P < 0.05) and the IR-group (115.6+/-11.8 pmol insulin per mmol glucose; P = 0.05). Furthermore, the acute insulin response during the first 10 min of an intravenous glucose tolerance test was lower in the IS-group than in the IR-group. Maximal insulin secretion capacity evaluated by C-peptide levels during the hyperglycemic clamp did not differ between the groups. The IR-group had lower rates of whole body glucose uptake (60.1+/-4.6 micromol per lean body mass per minute) than did the control group (84.2+/-5.0 micromol per lean body mass per minute; P < 0.001) or the IS-group (82.6+/-5.9 micromol per lean body mass per minute; P < 0.01) and this was due to reduced glucose nonoxidation. To conclude, both impaired insulin secretion and insulin action seem to be inherited and could represent the primary defects in glucose metabolism in the offspring of NIDDM probands.

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  • Version 1 (January 1, 1998): No description

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