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HOME > Diabetes Metab J > Volume 27(1); 2003 > Article
Original Article Impaired Insulin Secretion in Normoglycemic Offspring of Patients with Type 2 Diabetes.
Eun Kyung Byun, Young Sun Hong, Jee Young Oh, Yeon Ah Sung, Yeon Jin Jang
Diabetes & Metabolism Journal 2003;27(1):39-48
DOI: https://doi.org/
Published online: February 1, 2003
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1Department of Internal Medicine, Ewha Womans University College of Medicine, Korea.
2Department of Physiology, University of Ulsan College of Medicine, Seoul, Korea.

BACKGROUND
Although it is well known that insulin secretory defects and insulin resistance are major pathogenetic factors of type 2 diabetes, their relative importance still remains controversial in various ethnic groups. Increased levels of proinsulin, and the proinsulin/insulin (PI/I) ratio, are considered markers of pancreatic dysfunction, and predictors for the development of type 2 diabetes. To reveal which pathogenetic abnormality is most prominent in Koreans with type 2 diabetes, we measured the insulin sensitivity and secretory capacity in the normal glucose tolerant offspring of patients with type 2 diabetes. METHODS: Sixty-two offspring, with normal glucose tolerance (mean age 40.4+/-6.5 BMI 23.4+/-2.7 kg/m2), of type 2 diabetes parents, were compared with and 20, age and BMI-matched control subjects, with on family history of diabetes. We measured the serum levels of proinsulin (PI), specific insulin (I), and C-peptide(C) and calculated the PI/I and C/I ratios, as parameters of hepatic insulin clearance. The insulin sensitivity index (SI) was measured by the intravenous glucose tolerance test (IVGTT) using the MINMOD program, as a marker of insulin sensitivity. The acute insulin response to glucose (AIRg), AIRg by product, SI and the area under the insulin curve (AUCinsulin) were measured by IVGTT, and used as a marker of the insulin secretory capacity. We also evaluated the association between the proinsulin and insulin secretory capacities. RESULTS: Offspring of the type 2 diabetic patients had significantly lower AIRg SI and AUCinsulin (p<0.05), and tended to have lower AIRg (p=0.06), than the control subjects. However, there was no significant difference in the SI between the two groups. However, with the proinsulin, and the insulin, PI/I and C/I ratios, not significant differences were found between the offspring and the control subjects, and the PI/I ratio was not correlated with AIRg, AIRg x SI or SI. CONCLUSION: Insulin secretory defect could be a more prominent factor in the development of type 2 diabetes in Koreans, with no change in the proinsulin secretion.

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    Impaired Insulin Secretion in Normoglycemic Offspring of Patients with Type 2 Diabetes.
    Korean Diabetes J. 2003;27(1):39-48.   Published online February 1, 2003
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