Department of Epidemiology and Public Health, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Int J Obes (Lond). 2012 Aug;36(8):1086-93. doi: 10.1038/ijo.2011.185. Epub 2011 Sep 27.
Diabetes in Asia constitutes approximately half of the global burden. Although insulin resistance and incidence of type 2 diabetes differ substantially between ethnic groups within Asia, the reasons for these differences are poorly understood. We evaluated to what extent body fatness, adiponectin levels and inflammation mediate the relationship between ethnicity and insulin resistance in an Asian setting.
Cross-sectional population-based study.
In total, 4136 adult Chinese, Malays and Asian Indians residing in Singapore.
Insulin resistance was assessed using homeostasis model assessment (HOMA-IR) and systemic inflammation by C-reactive protein (CRP). Data were analyzed using path analysis.
HOMA-IR was highest in Asian Indians, intermediate in Malays and lowest in Chinese (P<0.001). The difference in HOMA-IR between Malays and Chinese disappeared after adjusting for body mass index (BMI). For the comparison of Asian Indians with Chinese, the association between ethnicity and HOMA-IR was mediated by BMI (men: 32.9%; women: 48.5%), BMI-adjusted waist circumference (men: 6.1%; women: 3.5%), and CRP (men: 5.1%; women: 5.6%), and unidentified factors (men: 47.2%; women: 26.5%). Part of the mediating effects of body fatness was indirect through effects of body fatness on CRP and adiponectin concentrations.
Mediators of ethnic differences in insulin resistance differed markedly depending on the ethnic groups compared. General adiposity explained the difference in insulin resistance between Chinese and Malays, whereas abdominal fat distribution, inflammation and unexplained factors contributed to excess insulin resistance in Asian Indians as compared with Chinese and Malays. These findings suggest that interventions targeting excess weight gain can reduce ethnic disparities in insulin resistance among Asian Indians, Chinese and Malays.
亚洲的糖尿病占全球负担的近一半。尽管亚洲不同种族之间的胰岛素抵抗和 2 型糖尿病的发病率存在显著差异，但这些差异的原因仍知之甚少。我们评估了在亚洲人群中，体脂含量、脂联素水平和炎症在多大程度上介导了种族与胰岛素抵抗之间的关系。
横断面人群基础研究。
新加坡的 4136 名成年华裔、马来裔和印度裔。
使用稳态模型评估（HOMA-IR）评估胰岛素抵抗，使用 C 反应蛋白（CRP）评估全身炎症。采用路径分析进行数据分析。
HOMA-IR 在印度裔中最高，在马来裔中居中，在华裔中最低（P<0.001）。调整体重指数（BMI）后，马来裔和华裔之间的 HOMA-IR 差异消失。对于印度裔与华裔的比较，种族与 HOMA-IR 之间的关联通过 BMI（男性：32.9%；女性：48.5%）、BMI 调整后的腰围（男性：6.1%；女性：3.5%）和 CRP（男性：5.1%；女性：5.6%）以及未确定因素（男性：47.2%；女性：26.5%）来介导。体脂含量的部分中介作用是通过体脂含量对 CRP 和脂联素浓度的影响间接产生的。
根据比较的种族群体的不同，胰岛素抵抗的种族差异的介导因素有很大差异。一般肥胖解释了华裔和马来裔之间胰岛素抵抗的差异，而腹部脂肪分布、炎症和未确定因素导致印度裔的胰岛素抵抗高于华裔和马来裔。这些发现表明，针对体重增加的干预措施可以减少印度裔、华裔和马来裔之间的胰岛素抵抗的种族差异。
