Abstract
In this article, we introduce the increasing prevalence of type 2 diabetes in the Japanese population and discuss the reasons for such an explosive increase. Diabetes has been brought into prominence in Japan by enhanced insulin resistance, through the change of lifestyle against the background of fragile β-cell function and thrifty genotypes.
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References and Recommended Reading
Health, Labour and Welfare Association, Ministry of Health: Annual Japanese Health, Labour and Welfare Statistics 2002. [in Japanese]. http://www.mhlw.go.jp/shingi/2004/03/s0318-15.html. Accessed March 2005.
Saad MF, Knowler WC, Pettitt DJ, et al.: A two-step model for development of non-insulin-dependent diabetes. Am J Med 1991, 90:229–235.
Torrens JI, Santoro N, Skurnick J, et al.: Ethnic differences in insulin sensitivity and beta-cell function in premenopausal or early perimenopausal women without diabetes: the Study of Women's Health Across the Nation (SWAN). Diabetes Care 2004, 27:354–361.
Kuroe A, Fukushima M, Usami M, et al.: Impaired beta-cell function and insulin sensitivity in Japanese subjects with normal glucose tolerance. Diabetes Res Clin Pract 2003, 59:71–77.
Tanaka Y, Matsuoka K, Atsumi Y, et al.: Usefulness of revised fasting plasma glucose criterion and characteristics of the insulin response to an oral glucose load in newly diagnosed Japanese diabetic subjects. Diabetes Care 1998, 21:1133–1137. Describes the characteristics of insulin secretion in the Japanese population.
Kanauchi M, Nakajima M, Kanauchi K: Pancreatic beta-cell function and insulin sensitivity in Japanese subjects with impaired glucose tolerance and newly diagnosed type 2 diabetes mellitus. Metabolism 2003, 52:476–481.
Matsumoto K, Yamaguchi Y, Miyake S, et al.: Glucose tolerance, insulin secretion, and insulin sensitivity in nonobese and obese Japanese subjects. Diabetes Care 1997, 20:1562–1568.
Sato Y, Komatsu M, Katakura M, et al.: Diminution of early insulin response to glucose in subjects with normal but minimally elevated fasting plasma glucose. Evidence for early beta-cell function. Diabet Med 2002, 19:566–571.
Suzuki H, Fukushima M, Usami M, et al.: Factors responsible for development from normal glucose tolerance to isolated postchallenge hyperglycemia. Diabetes Care 2003, 26:1211–1215.
Hirose T, Mizuno R, Yoshimoto R: The effects of nateglinide following oral glucose load in impaired glucose tolerance subjects: rapid insulin stimulation by nateglinide in IGT subjects. Endocr J 2002, 49:649–652.
Uchino H, Niwa M, Shimizu T, et al.: Impairment of early insulin response after glucose load rather than insulin resistance, is obese type 2 diabetes: assessment using nateglinide, a new insulin secretagogue. Endocr J 2000, 47:639–641.
Kawamori R: Diabetes trends in Japan. Diabetes Metab Res Rev 2002, 18:S9-S13.
Yamada M, Wong FL, Kodama K, et al.: Longitudinal trends in total serum cholesterol levels in a Japanese cohort, 1958–1986. J Clin Epidemiol 1997, 50:425–434.
Suematsu C, Hayashi T, Fujii S, et al.: Impaired fasting glucose and the risk of hypertension in Japanese men between the 1980s and the 1990s. The Osaka Health Survey. Diabetes Care 1999, 22:228–232.
Todoroki I, Shinchi K, Kono S, et al.: Lifestyle and glucose tolerance: a cross-sectional study of Japanese men. Ann Epidemiol 1994, 4:363–368.
Sugimori H, Miyakawa M, Yoshida K, et al.: Health risk assessment for diabetes mellitus based on longitudinal analysis of MHTS database. J Med Syst 1998, 22:27–32.
Watanabe H, Yamane K, Fujikawa R, et al.: Westernization of lifestyle markedly increase carotid intima-media wall thickness (IMT) in Japanese people. Atherosclerosis 2003, 166:67–72.
Sone H, Katagiri A, Ishibashi S, et al.: Effects of lifestyle modifications on patients with type 2 diabetes: the Japan Diabetes Complications Study (JDCS) study design, baseline analysis and three-year interim report. Horm Metab Res 2002, 34:509–515. Describes an interim report on effects of lifestyle modifications on patients with type 2 diabetes in the Japanese population.
Evans RM: The steroid and thyroid receptor superfamily. Science 1988, 240:889–895.
Torra IP, Chinetti G, Duval C, et al.: Peroxisome proliferatoractivated receptors: from transcriptional control to clinical practice. Curr Opin Lipidol 2001, 12:245–254.
Kersten S, Desvergne B, Wahli W: Roles of PPARs in health and disease. Nature 2000, 405:421–424.
Ricote M, Li AC, Willson TM, et al.: The peroxisome proliferator-activated receptor gamma is a negative regulator of macrophage activation. Nature 1998, 391:79–82.
Staels B, Koenig W, Habib A, et al.: Activation of human aortic smooth-muscle cells is inhibited by PPAR alpha but not by PPAR gamma activators. Nature 1998, 393:790–793.
Yen CJ, Beamer BA, Negri C, et al.: Molecular scanning of the human peroxisome proliferator activated receptor gamma gene in diabetic Caucasians: identification of a Pro 12Al PPAR gamma 2 missense mutation. Biochem Biophys Res Commun 1997, 241:270–274.
Hara K, Okada T, Tobe K, et al.: The Pro 12Ala polymorphism in PPAR gamma2 may confer resistance to type 2 diabetes. Biochem Biophys Res Commun 2000, 271:212–216.
Mori H, Ikegami H, Kawaguchi Y, et al.: The Pro 12 Ala substitution in PPAR-gamma is associated with resistance to development of diabetes in the general population: possible involvement in impairment of insulin secretion in individuals with type 2 diabetes. Diabetes 2001, 50:891–894.
Garcia-Rubi E, Calles-Escandon J: Insulin resistance and type 2 diabetes mellitus: its relationship with the beta 3-adrenergic receptor. Arch Med Res 1999, 30:459–464.
Azuma N, Yoshimasa Y, Nishimura H, et al.: The significance of the Trp 64 Arg mutation of the beta3-adrenergic receptor gene in impaired glucose tolerance, non-insulin-dependent diabetes mellitus, and insulin resistance in Japanese subjects. Metabolism 1998, 47:456–460.
Matsushita H, Kurabayashi T, Tomita M, et al.: Effects of uncoupling protein 1 and beta3-adrenergic receptor gene polymorphisms on body size and serum lipid concentration in Japanese women. Maturitas 2003, 45:39–45.
Nakajima S, Baba T: Trp64Arg polymorphism of the beta3-adrenergic receptor is not associated with diabetic nephropathy in Japanese patients with type 2 diabetes. Diabetes Care 2000, 23:862–863.
Kahara T, Takamura T, Hayakaawa, et al.: Prediction of exercise-mediated changes in metabolic markers by gene polymorphism. Diabetes Res Clin Pract 2002, 57:105–110.
Baier LJ, Permana PA, Yang X, et al.: A calpain-10 gene polymorphism is associated with reduced muscle mRNA levels and insulin resistance. J Clin Invest 2000, 106:R69-R73.
Daimon M, Oizumi T, Saitoh T, et al.: Calpain 10 gene polymorphisms are related, not to type 2 diabetes, but to increased serum cholesterol in Japanese. Diabetes Res Clin Pract 2002, 56:147–152.
Horikawa Y, Oda N, Yu L, et al.: Genetic variations in calpain-10 gene are not a major factor in the occurrence of type 2 diabetes in Japanese. J Clin Endocrinol Metab 2003, 88:244–247.
Rasmussen SK, Urhammer SA, Berglund L, et al.: Variant within the calpain-10 gene on chromosome 2q37 (NIDDM) and relationships to type 2 diabetes, insulin resistance and impaired acute insulin secretion among Scandinavian Caucasians. Diabetes 2002, 51:3561–3567.
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Hirose, T., Kawamori, R. Diabetes in Japan. Curr Diab Rep 5, 226–229 (2005). https://doi.org/10.1007/s11892-005-0013-4
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DOI: https://doi.org/10.1007/s11892-005-0013-4