Korean Diabetes Journal 2000;24(3):356-364.
Published online January 1, 2001.
Insulin Secretion and Insulin Sensitivity in Korean Subjects with Impaired Glucose Intolerance.
Dong Jun Kim, Jong Ryul Hahm, In Kyoung Jeong, Tae Young Yang, Eun Young Oh, Yoon Ho Choi, Jae Hoon Chung, Yong Ki Min, Myung Shik Lee, Moon Kyu Lee, Kwang Won Kim
1Division of Endocrinology and Metabolism, Samsung Medical Center, Sungkyunkwan University School of Medicine.
2Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine.
3Health Promotion Center, Samsung Medical Center, Sungkyunkwan University School of Medicine.
4Department of Internal Medicine, Ilsan Paik Hospital, Inje University College of Medicine.
5Department of Internal Medicine, Gyeongsang National University College of Medicine.
Although insulin resistance has been known to be a primary defect causing type 2 diabetes in Pima Indians and Caucasians. However, insulin secretory defect rather than insulin resistance has been speculated and demonstrated to be a more important factor in the development of type 2 diabetes in other ethnic groups. Thus, we undertook this study to investigate the initial abnormality of glucose intolerance in Korean subjects. METHODS: 374 Korean subjects were stratified according to the World Health Organization criteria (normal glucose tolerance [NGT], n = 128; impaired glucose tolerance [IGT], n=128; diabetes, n=118) and subdivided further into the two groups; non-obese (BMI < 25 kg/m2) and obese group (BMI 25 kg/m2). Insulinogenic index (the ratio of the increment of insulin to that of plasma glucose 30 min after glucose load) was used as an index of early-phase insulin secretion. AUC insulin (area under the insulin curve during OGTT) was used as an index of total insulin secretion. Insulin resistance was assessed by HOMA (R), the R value of the Homeostasis model. RESULTS: Insulinogenic index decreased significantly in IGT compared with that in NGT in both non-obese and obese groups, respectively. There was no significant difference in AUC insulin and HOMA (R) between NGT and IGT group. WhereasAUC insulin showed its peak level in the range of IGT (7.7~9.9 mmol/L), insulinogenic index showed the peak level in the range of NGT (5.6~7.7 mmol/lL and decreased progressively with increase of plasma glucose 120 min value. CONCLUSION: Early-phase insulin secretory defect might be the initial abnormality in the development of IGT from NGT in both non-obese and obese Korean subjects.
Key Words: Insulin secretion, Insulin resistance, HOMA(R), Insulinogenic index

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