Abstract
The prevalence of diabetes mellitus(DM) is increasing in Korea and is estimated at 7~8%. This high prevalence is most likely the result of a complex interaction between genetic and environmental factors. The lifestyle and diet of the Korean population have changed significantly during the last several decades. In general, the Koreans have become more sedentary and they consume westernized diet. In addition to the increase of prevalence, the clinical characteristics of DM in Korea are somewhat different from those in Western countries. The incidence rate of type 1 DM in Korea is one of the lowest reported in the world. There are many patients with atypical type 1 or type 2 DM, initially classified into type 2 DM but requiring insulin eventually. There are many patients with non-obese type 2 DM, and many of them lose weight significantly during the course of disease. In addition, some patients with type 2 DM have autoantibodies to the beta cell-specific antigen. The defect in insulin secretion is prominent in non-obese subjects with impaired glucose tolerance or early phase of type 2 DM. The Korean patients with type 2 DM have a markedly decreased beta cell mass. The impaired insulin secretion may play a role in the pathogenesis of non-obese type 2 DM in Korea. Of note, similar features are also observed in Japanese patients. Unfortunately, there are few studies that evaluated the pathogenesis and clinical characteristics of Korean patients with DM, particularly in a cohort-based prospective manner.
References
1. Ko Kw, Sw Yang, Nh Cho. The incidence of IDDM in Seoul from 1985 to 1988. Diabetes Care. 1994. 17:1473–1475.
2. Lee Hk, Ys Oh, Yh Chung, Hj Yoo, Sh Shin, Yk Choi, et al. Epidemiological characteristics of ketoacidosis among Korean diabetic patients. J Korean Med Sci. 1987. 2:7–11.
5. Lee Ku, Kim Sw, Park Jy, Ko Ks, Rhee Bd, Min Hk. Clinical heterogeneity of insulin dependent diabetes mellitus in Korea. Diabetes Res Clin Pract. 1995. 27:159–162.
6. Park Ys, Kawasaki E, Kelemen K, Yu L, Schiller Mr, Hutton Jc, et al. Humoral autoreactivity to an alternatively spliced variant of ICA512/IA-2 in Type I diabetes. Diabetologia. 2000. 43:1293–1301.
8. Buzzetti R, Nistico L, Osborn J, Giovannini C, Chersi A, Sorrentino R. HLA-DQA1 and DQB1 gene polymorphisms in type I diabetic patients from central Italy and their use for risk prediction. Diabetes. 1993. 42:1173–1178.
9. Kida K, Mimura G, Kobayashi T, Nakamura K, Sonoda S, Tsuji K, et al. Immunogenetic heterogeneity in type 1 (insulin-dependent) diabetes among Japanese HLA antigens and organ-specific autoantibodies. Diabetologia. 1989. 32:34–39.
10. Sugihara S, Sakamaki T, Konda S, Murata A, Wataki K, Niimi H, et al. Association of HLA-DR, DQ genotype with different beta-cell functions at IDDM diagnosis in Japanese children. Diabetes. 1997. 46:1893–1897.
19. Rifkin H Pjd, editor. Diabetes Mellitus; Theory and Practice. 1990. New York: Elsevier.
20. Zimmet P, Dowse G, Finch C, Serjeantson S, King H. The epidemiology and natural history of NIDDM-lessons from the South Pacific. Diabetes Metab Rev. 1990. 6:91–124.
21. Saad Mf, Knowler Wc, Pettitt Dj, Nelson Rg, Charles Ma, Bennett Ph. A two-step model for development of non-insulin-dependent diabetes. Am J Med. 1991. 90:229–235.
22. Warram Jh, Martin Bc, Krolewski As, Soeldner Js, Kahn Cr. Slow glucose removal rate and hyperinsulinemia precede the development of type II diabetes in the offspring of diabetic parents. Ann Intern Med. 1990. 113:909–915.
23. Gulli G, Ferrannini E, Stern M, Haffner S, Defronzo Ra. The metabolic profile of NIDDM is fully established in glucose-tolerant offspring of two Mexican-American NIDDM parents. Diabetes. 1992. 41:1575–1586.
24. Martin Bc, Warram Jh, Krolewski As, Bergman Rn, Soeldner Js, Kah Cr. Role of glucose and insulin resistance in development of type 2 diabetes mellitus: results of a 25-year follow-up study. Lancet. 1992. 340:925–929.
25. Pimenta W, Mitrakou A, Jensen T, Yki-Jarvinen H, Daily G, Gerich J. Insulin secretion and insulin sensitivity in people with impaired glucose tolerance. Diabet Med. 1996. 13:9 Suppl 6. 33–36.
26. Yoneda H, Ikegami H, Yamamoto Y, Yamato E, Cha T, Ogihara T, et al. Analysis of early-phase insulin responses in nonobese subjects with mild glucose intolerance. Diabetes Care. 1992. 15:1517–1521.
27. Matsumoto K, Miyake S, Yano M, Ueki Y, Yamaguchi Y, Tominaga Y, et al. Glucose tolerance, insulin secretion, and insulin sensitivity in nonobese and obese Japanese subjects. Diabetes Care. 1997. 20:1562–1568.
28. Doi K, Taniguchi A, Nakai Y, Kawamura H, Higaki Y, Fukushima M, et al. Decreased glucose effectiveness but not insulin resistance in glucose-tolerant offspring of Japanese non-insulin-dependent diabetic patients: a minimal-model analysis. Metabolism. 1997. 46:880–883.
33. Yoon Kh, Ko Sh, Cho Jh, Lee Jm, Ahn Yb, Bonner-Weir S, et al. Selective beta-cell loss and alpha-cell expansion in patients with type 2 diabetes mellitus in Korea. J Clin Endocrinol Metab. 2003. 88:2300–2308.
36. Reaven Gm, Chen Yd, Hollenbeck Cb, Sheu Wh, Ostrega D, Polonsky Ks. Plasma insulin, C-peptide, and proinsulin concentrations in obese and nonobese individuals with varying degrees of glucose tolerance. J Clin Endocrinol Metab. 1993. 76:44–48.