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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.
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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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Byun EK, Hong YS, Oh JY, Sung YA, Jang YJ. Impaired Insulin Secretion in Normoglycemic Offspring of Patients with Type 2 Diabetes.. Diabetes Metab J. 2003;27(1):39-48.
DOI: https://doi.org/.

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