Central obesity insulin resistance syndrome X lipoprotein(a) and cardiovascular risk in Indians Malays and Chinese in Singapore.

摘要

STUDY OBJECTIVE: To examine the hypothesis that the higher rates of coronary heart disease (CHD) in Indians (South Asians) compared with Malays and Chinese is at least partly explained by central obesity, insulin resistance, and syndrome X (including possible components). DESIGN: Cross sectional study of the general population. SETTING: Singapore. PARTICIPANTS: Random sample of 961 men and women (Indians, Malays, and Chinese) aged 30 to 69 years. MAIN RESULTS: Fasting serum insulin concentration was correlated directly and strongly with body mass index (BMI), waist-hip ratio (WHR), and abdominal diameter. The fasting insulin concentration was correlated inversely with HDL cholesterol and directly with the fasting triglyceride concentration, blood pressures, plasminogen activator inhibitor 1 (PAI-1), and tissue plasminogen activator (tPA), but it was not correlated with LDL cholesterol, apolipoproteins B and A1, lipoprotein(a), (Lp(a)), fibrinogen, factor VIIc, or prothrombin fragment (F)1 + 2. This indicates that the former but not the latter are part of syndrome X. While Malays had the highest BMI, Indians had a higher WHR (men 0.93 and women 0.84) than Malays (men 0.91 and women 0.82) and Chinese (men 0.91 and women 0.82). In addition, Indians had higher fasting insulin values and more glucose intolerance than Malays and Chinese. Indians had lower HDL cholesterol, and higher PAI-1, tPA, and Lp(a), but not higher LDL cholesterol, fasting triglyceride, blood pressures, fibrinogen, factor VIIc, or prothrombin F1 + 2. CONCLUSIONS: Indians are more prone than Malays or Chinese to central obesity with insulin resistance and glucose intolerance and there are no apparent environmental reasons for this in Singapore. As a consequence, Indians develop some but not all of the features of syndrome X. They also have higher Lp(a) values. All this puts Indians at increased risk of atherosclerosis and thrombosis and must be at least part of the explanation for their higher rates of CHD.