Type 2 (non-insulin-dependent) diabetes mellitus and insulin resistance are associated with centrally-distributed obesity. These disturbances are especially prevalent in people of South Asian (Indian, Pakistani and Bangladeshi) descent. We examined the relationship of glucose intolerance to body fat pattern in a population survey of 2936 men and 537 women of South Asian and European origin living in London, UK. In both groups glucose intolerance (defined as diabetes or impaired glucose tolerance) was more strongly associated with waist-hip girth ratio than with skinfolds or body mass index. The associations between body mass index and glucose intolerance were fully accounted for by waist-hip ratio. In European men with normal glucose tolerance fasting insulin levels were more strongly correlated with body mass index than with waist-hip ratio. Physical activity scores were lower in South Asians than in Europeans but no statistically significant associations between glucose intolerance and low physical activity were detectable. Leisure-time physical activity scores were inversely correlated with 2 h insulin levels in both groups. In contrast with other studies these results suggest that a specific effect of intra-abdominal fat deposition underlies the association between glucose intolerance and obesity. The association between hyperinsulinaemia and obesity is less specific for centrally-distributed fat. When measured appropriately waist-hip ratio is the most valid anthropometric index for identifying individuals whose obesity predisposes them to glucose intolerance.
"However, some have suggested that BMI has a relatively weak association with chronic disease prevalence   and with visceral abdominal fat  in AI. As alternative measures, studies in various populations, including AI [9, 22–24], US , and elsewhere , suggest that either waist circumference (WC) alone   or waist-hip ratio (WHR)     may be a better single anthropometric marker of chronic disease risk, as compared to BMI, because they may more specifically reflect abdominal body fatness. However, WC alone does not reflect lean body mass, which is known to be protective , and fails to allow comparisons between subjects and populations due to confounding by body size and weight. "
[Show abstract][Hide abstract] ABSTRACT: Background:
Relative to Europeans, Asian Indians have higher rates of type 2 diabetes and cardiovascular disease. Whether differences in body composition may underlie these population differences remains unclear.
We compared directly measured anthropometric data from the Chennai Urban Rural Epidemiology Study (CURES) survey of southern Indians (I) with those from three US ethnic groups (C: Caucasians, A: African Americans, and M: Mexican Americans) from NHANES III (Third National Health and Nutrition Examination Survey). A total of 15,733 subjects from CURES and 5,975 from NHANES III met inclusion criteria (age 20-39, no known diabetes).
Asian Indian men and women had substantially lower body mass index, waist circumference, hip circumference, waist-to-hip ratio, and body surface area relative to US groups (P values <0.0001). In contrast, the mean (±se) waist-weight ratio was significantly higher (P < 0.001) in I (men 1.35 ± 0.002 and women 1.45 ± 0.002) than in all the US groups (1.09, 1.21, and 1.14 in A, M, and C men; 1.23, 1.33, and 1.26 in A, M, and C women (se ranged from 0.005 to 0.006)).
Compared to the US, the waist-weight ratio is significantly higher in men and women from Chennai, India. These results support the hypothesis that Southeast Asian Indians are particularly predisposed toward central adiposity.
Journal of obesity 09/2014; 2014:461956. DOI:10.1155/2014/461956
"Indians are one of the ethnic groups that are considered to be a high‐risk population for diabetes3. Compared with Europeans, Indians have greater insulin resistance capability5, which promotes susceptibility to diabetes8. This is indicative of a strong genetic predisposition to type 2 diabetes mellitus in Indians. "
[Show abstract][Hide abstract] ABSTRACT: Aims/IntroductionPeroxisome proliferator activated receptor gamma (PPARG) is a nuclear hormone receptor of the ligand-dependent transcription factor involved in adipogenesis, and a molecular target of the insulin sensitizer, thiazolidinediones. The present study aimed to investigate whether the PPARG gene is associated with type 2 diabetes mellitus and its related traits within the population of West Bengal, India. Materials and Methods
The study participants (200 type 2 diabetes mellitus and 200 normal individuals) were chosen randomly, and the variants were screened by direct sequencing. ResultsThe results showed that rs1801282 (odds ratio 0.66; 95% confidence interval 0.15–2.96; P = 0.57) and rs3856806 (odds ratio 1.23; 95% confidence interval 0.73–2.06; P = 0.44) variants of the PPARG gene were not associated with type 2 diabetes mellitus. Conclusions
The results showed that the PPARG gene was not associated with type 2 diabetes mellitus in our study population. As the lack of association might come from the small sample size, further studies with larger sample size are required to verify the present observation.
"There is a well known association between obesity and T2DM, but South Asians develop T2DM at lower levels of body mass index (BMI) than Westerners, and are more insulin resistant for any given BMI
[12,13]. Several studies have indicated that, in individuals from South Asia, BMI may be inferior to other measures of adiposity as a predictor of metabolic risk
[Show abstract][Hide abstract] ABSTRACT: Immigrants from South Asia to Western countries have a high prevalence of type 2 diabetes mellitus (T2DM). We explored pathogenic factors that might contribute to the high risk of T2DM in Pakistani immigrants to Norway.
A cross-sectional study was performed in 18 Pakistani and 21 Norwegian men and women with T2DM (age 29 -- 45 years), recruited from two hospital out-patient clinics. Anthropometrics and a two-step euglycemic, hyperinsulinemic clamp with measurements of non-esterified fatty acids (NEFA) during clamp, was performed in all patients. Insulin sensitivity, given as the Glucose Infusion Rate (GIR) and Insulin Sensitivity Index (ISI), was calculated from the two euglycemic clamp steps. Fasting adipokines and inflammatory mediators were measured. Continuous variables between groups were compared using Student's t test or Mann--Whitney U test as appropriate. Spearman's correlation coefficient and multiple linear regression analyses were used.
Despite having a lower BMI, Pakistani patients were more insulin resistant than Norwegian patients, during both low and high insulin infusion rates, after adjustment for sex and % body fat: median (interquartile range) GIR(low insulin): 339.8(468.0) vs 468.4(587.3) mumol/m2/min (p = 0.060), ISI(low insulin): 57.1(74.1) vs 79.7(137.9) mumol/m2/min (p = 0.012), GIR(high insulin): 1661.1(672.3) vs 2055.6(907.0) mumol/m2/min (p = 0.042), ISI(high insulin): 14.2(7.3) vs 20.7(17.2) mumol/m2/min (p = 0.014). Pakistani patients had lower percentage NEFA suppression 30 minutes into clamp hyperinsulinemia than Norwegians: 41.9(90.6)% vs 71.2(42.1)%, (p = 0.042). The relationship of ISI to BMI, leptin and interleukin-1 receptor antagonist also differed between Norwegians and Pakistanis.
Compared with Norwegian patients, Pakistani patients with T2DM had lower insulin sensitivity, affecting both glucose and lipid metabolism. The relation of insulin sensitivity to BMI and some adipokines also differed between the groups.
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