The prevalence of cardiovascular disease (CVD) risk factors in "People of Indian Origin" (PIO) is exceedingly high and strong relationships among elevated blood pressure, increased levels of lipoproteins, visceral obesity, physical inactivity and subsequent high occurrence of coronary heart disease, type 2 diabetes mellitus etc., were evident in many studies. Increasing urbanization with effective changes in lifestyles could be attributed to explain this exaggerated rate. The present community based cross-sectional investigation was aimed to identify rural-urban differences in prevalence of risk factors of CVD in the adult Asian Indians. A total of 350 adult (30 years and above) individuals (184 males and 166 females) belong to urban (n = 193, males = 104, and females = 89) and rural (n = 157, males = 80, and females = 77) areas participated in the study. Anthropometric measures, lipids profiles, fasting blood glucose and blood pressure measures were obtained from participants. The mean body mass index (kg/m2) for male and female was 22.37 +/- 4.09 and 23.20 +/- 4.37, respectively. There existed significant differences for anthropometric, metabolic, and blood pressure variables between rural and urban areas. Habitat (rural vs. urban) had significant impact on central adiposity, lipids, lipoproteins, and blood pressure measures even after adjusted for age and sex. Overall, 84.3% of females had lower HDL level compared with only 20.1% in males. It was also observed that the prevalence of metabolic syndrome was 56.2% in urban females compared with 36.4% in rural females. Effective urbanization and or modernization seem to influence CVD risk factors and warrants intervention as early as adulthood to check this menace.

Background:Our objective was to test the association between familial risk of type 2 diabetes mellitus (T2DM) and the prevalence of metabolic syndrome (MS) in adult Asian Indians.Materials and Methods:A total of 448 adult (>30 years) individuals (257 males and 191 females) participated in the study. Familial risk of T2DM was classified into three groups viz., 1=both parents affected; 2=parent and/or siblings affected and 3=none or no family history for T2DM. Anthropometric measures, blood pressures, fasting blood glucose and metabolic profiles were studied using standard techniques. MS was defined accordingly. The prevalence of MS phenotypes was estimated and compared among the three familial risk strata.Results:Individuals with a history of both parents affected from diabetes had significantly higher (P<0.001) body mass index (BMI), waist circumference (WC), waist-hip ratio (WHR), systolic blood pressure (SBP), diastolic blood pressure (DBP) and fasting blood glucose (FBG; P=0.035) than individuals having no family history of T2DM. Significant difference was also noticed between individuals with and without MS according to the family history of diabetes (P<0.001). Differences were evident between individuals who fulfilled all the MS criteria (P=0.001) and individuals with only one or two criteria (phenotypes) according to family history of T2DM.Conclusion:Family history of T2DM had significant effect on individuals with MS as compared to their counterparts (individuals having no family history of T2DM). It therefore seems reasonable to argue that family history of T2DM could be useful as a predictive tool for early diagnosis and prevention of MS in Asian Indian population.

In this study, we conducted an epigenome-wide association study of metabolic syndrome (MetS) among 846 participants of European descent in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN). DNA was isolated from CD4+ T cells and methylation at ~470,000 cytosine-phosphate-guanine dinucleotide (CpG) pairs was assayed using the Illumina Infinium HumanMethylation450 BeadChip. We modeled the percentage methylation at individual CpGs as a function of MetS using linear mixed models. A Bonferroni-corrected P-value of 1.1 x 10−7 was considered significant. Methylation at two CpG sites in CPT1A on chromosome 11 was significantly associated with MetS (P for cg00574958 = 2.6x10-14 and P for cg17058475 = 1.2x10-9). Significant associations were replicated in both European and African ancestry participants of the Bogalusa Heart Study. Our findings suggest that methylation in CPT1A is a promising epigenetic marker for MetS risk which could become useful as a treatment target in the future.

Objective:The present community-based cross-sectional study was aimed to examine the association of metabolic syndrome (MS) with obesity measures, metabolic profiles, and intake of dietary fatty acids in Asian Indian population.Patients and Methods:A total of 350 adult (30 years and above) individuals (184 males and 166 females) inhabiting in and around Kolkata, India participated in this study. MS was defined using the protocol specifically designed for Asian Indian population.Results:The prevalence of MS in the study was 31.4%. The prevalence was significantly higher (P < 0.01) in females (48.2%) as compared to males (16.3%). It was observed that males without MS had significantly higher mean waist circumference (WC P < 0.05); waist–hip ratio (WHR; P < 0.001); triglyceride (TG; P < 0.05); very low density lipoprotein cholesterol (VLDLc; P < 0.05) and fasting blood glucose (FBG; P < 0.01) as compared to females without MS. Significant differences were also observed for dietary intake of total fatty acids (TFA; P < 0.001); saturated fatty acids (SFA; P < 0.001) and polyunsaturated fatty acids (PUFA; P < 0.001) between individuals with and without MS. However, no significant association was observed in individuals with MS after controlling for age and sex. On the other, WC and body mass index (BMI) had significant correlation with SFA: mono unsaturated fatty acids (MUFA; P < 0.01) in individuals without MS even after controlling for age and sex.Conclusion:It seem reasonable to argue that while dealing with MS in Asian Indians, clinicians should consider obesity measures, metabolic profiles and dietary fatty acids simultaneously.

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Fenofibrate lowers triglycerides (TG) and raises high density lipoprotein cholesterol (HDLc) in dyslipidemic individuals. Several studies have shown genetic variability in lipid responses to fenofibrate treatment. It is, however, not known whether epigenetic patterns are also correlated with the changes in lipids due to fenofibrate treatment. The present study was therefore undertaken to examine the changes in DNA methylation among the participants of Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) study. A total of 443 individuals were studied for epigenome-wide changes in DNA methylation, assessed using the Illumina Infinium HumanMethylation450 array, before and after a 3-week daily treatment with 160 mg of fenofibrate. The association between the change in DNA methylation and changes in TG, HDLc, and low-density lipoprotein cholesterol (LDLc) were assessed using linear mixed models adjusted for age, sex, baseline lipids, and study center as fixed effects and family as a random effect. Changes in DNA methylation were not significantly associated with changes in TG, HDLc, or LDLc after 3 weeks of fenofibrate for any CpG. CpG changes in genes known to be involved in fenofibrate response, e.g., PPAR-α, APOA1, LPL, APOA5, APOC3, CETP, and APOB, also did not show evidence of association. In conclusion, changes in lipids in response to 3-week treatment with fenofibrate were not associated with changes in DNA methylation. Studies of longer duration may be required to detect treatment-induced changes in methylation.

The angiotensin converting enzyme (ACE) gene insertion/deletion polymorphism has been identified as a potential genetic risk factor for essential hypertension. The purpose of the present study is to investigate the association of the insertion/deletion polymorphism of the ACE gene with essential hypertension in adult Asian Indians. Three hundred fifty (184 males and 166 females) adult (30 years and older) Asian Indians of Calcutta and its suburbs participated in this population-based cross-sectional study. Anthropometric measures, lipids profiles, blood glucose, and blood pressure measures were collected from participants. ACE insertion/deletion polymorphism was determined by agarose gel electrophoresis and D/D typing was further reconfirmed using insertion-allele-specific amplification. Essential hypertension was defined as a systolic blood pressure (SBP) greater than 160 mm Hg and/or a diastolic blood pressure (DBP) greater than 90 mm Hg or use of any antihypertensive treatment by participants. Significantly higher SBP, DBP, and mean arterial pressure were recorded in D/D subjects compared to I/I and I/D subjects. We also observed that the odds of being hypertensive were 7.483 (95% CI = 1.746, 30.192) in D/D individuals compared to those carrying one or no D alleles. This finding suggests that ACE insertion/deletion polymorphism is associated with essential hypertension in Asian Indians. Moreover, individuals who are homozygous for the D allele of the ACE gene are more likely to have essential hypertension.

No common underlying physiological variables in premenopausal and postmenopausal women indicate that a single risk axis for clustering of cardiometabolic phenotypes is highly unlikely.