Ethnicity and type 2 diabetes: Focus on Asian Indians
Introduction
The prevalence of diabetes, particularly type 2 diabetes, continues to increase in the US and in all westernized Countries. Over the past 40 years, a fivefold increase in the prevalence of type 2 diabetes has been observed in US. Because of the high associated morbidity and mortality, this trend obviously poses a public health threat. Similar trends are observed in developing countries where “westernization” of lifestyle is adopted. These observations clearly suggest that acquired/environmental factors inherent with “western” lifestyle play a significant role in the development of type 2 diabetes in a growing number of individuals. However, there is also growing evidence that some group of individuals or ethnicity have a particular “predisposition” to develop type 2 diabetes in the presence of adverse environmental conditions. In fact, epidemiological studies show that the prevalence of this disease is significantly higher in ethnic minorities such as the Hispanics and Asians as compared to the ethnic group of European descent (Caucasians) even when exposed to similar environmental condition Hanis et al., 1983, Ramachandran et al., 1992, Simmons et al., 1992, Stern et al., 1984. As shown in Fig. 1, an increasing prevalence of diabetes in our population is observed for all ethnic groups. However, Asians Americans have experienced the highest rate of increase in prevalence between the years 1990 and 1998. The changing ethnic composition of the US population and the progressive population enrichment with ethnic groups at high risk for diabetes, like the Asian Americans, may contribute significantly to the worsening diabetes epidemic in this country. Among the Asian Americans, immigrants from India, Pakistan, and Bangladesh (Asian Indians) have the highest predisposition to develop diabetes. Epidemiological data from India and other countries where Indians have migrated document the excessive predisposition to develop diabetes in this ethnic group. As shown in Fig. 2, whereas Asian Indians living in rural India have only 2–3% prevalence of diabetes (Ramachandran et al., 1992), those living in urban areas or migrated to developed countries experience about a fourfold increase in prevalence of diabetes Dowse et al., 1990, McKeigue et al., 1989. It has been estimated that the prevalence of type 2 diabetes in Asian Indians is about 19% vs. about 5% observed in the Caucasian. Since it is projected that by the year 2020 over 50% of the US population will include non-Caucasian ethnicity, and since the new migration greatly involves subjects of Asian Indian descent, the gaps in the health of minority populations in the US will certainly worsen. Therefore, the identification of the mechanisms involved in the development of excessive type 2 diabetes in ethnic minorities like the Asian Indians becomes a public health priority.
Section snippets
Pathogenesis of type 2 diabetes in Asian Indians
To understand ethnic differences in predisposition to diabetes, mechanistic evaluation of pathogenesis of diabetes has to be evaluated in the various ethnicities. The pathogenesis of type 2 diabetes involves both β-cell dysfunction and insulin resistance. There is evidence, however, that the relative contribution of these two pathogenetic factors is different in the various ethnic groups. For example, in African Americans, β-cell dysfunction rather than insulin resistance has been reported to
Etiology of insulin resistance in Asian Indians
Interethnic differences in insulin resistance may have an environmental or genetic explanation. The main acquired factors that seemingly increase insulin resistance in all ethnic groups include obesity, sedentary lifestyle, diet rich in animal products, and aging. Among these different environmental determinants of insulin resistance, nutrition, lack of exercise, and obesity may be part of the so-called westernization process in migrant Asian Indians, which can induce excessive insulin
Mechanisms of interaction between obesity and insulin resistance
Although the details of the mechanisms involved in the development of insulin resistance are still incompletely understood, an increasing body of scientific data is being accumulated on the effects of obesity on specific molecular mechanisms related to cellular insulin signaling. Obese human subjects have decreased insulin receptor expression and decreased tyrosine kinase activity in skeletal muscle cells (Caro et al., 1987) and adipocytes (Olefsky, 1976). Insulin receptor expression is
Diet and exercise
Reduction in dietary fats and caloric intake will promote weight control and reduce insulin resistance. Dietary composition may independently affect insulin resistance. Regular exercise increases the number of capillaries surrounding muscle fibers and also increases the skeletal muscle fiber composition that favors insulin-mediated glucose disposal (Utriainen et al., 1996). Bouts of exercise stimulate translocation of GLUT-4 to the plasma membrane and increase glucose transport in skeletal
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