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To study the pattern and prevalence of dyslipidemia in a large representative sample of four selected regions in India. Phase I of the Indian Council of Medical Research-India Diabetes (ICMR-INDIAB) study was conducted in a representative population of three states of India [Tamil Nadu, Maharashtra and Jharkhand] and one Union Territory [Chandigarh], and covered a population of 213 million people using stratified multistage sampling design to recruit individuals ≥20 years of age. All the study subjects (n = 16,607) underwent anthropometric measurements and oral glucose tolerance tests were done using capillary blood (except in self-reported diabetes). In addition, in every 5th subject (n = 2042), a fasting venous sample was collected and assayed for lipids. Dyslipidemia was diagnosed using National Cholesterol Education Programme (NCEP) guidelines. Of the subjects studied, 13.9% had hypercholesterolemia, 29.5% had hypertriglyceridemia, 72.3% had low HDL-C, 11.8% had high LDL-C levels and 79% had abnormalities in one of the lipid parameters. Regional disparity exists with the highest rates of hypercholesterolemia observed in Tamilnadu (18.3%), highest rates of hypertriglyceridemia in Chandigarh (38.6%), highest rates of low HDL-C in Jharkhand (76.8%) and highest rates of high LDL-C in Tamilnadu (15.8%). Except for low HDL-C and in the state of Maharashtra, in all other states, urban residents had the highest prevalence of lipid abnormalities compared to rural residents. Low HDL-C was the most common lipid abnormality (72.3%) in all the four regions studied; in 44.9% of subjects, it was present as an isolated abnormality. Common significant risk factors for dyslipidemia included obesity, diabetes, and dysglycemia. The prevalence of dyslipidemia is very high in India, which calls for urgent lifestyle intervention strategies to prevent and manage this important cardiovascular risk factor.

Common variants of fat mass and obesity-associated gene ( FTO , fat mass- and obesity-associated gene) have been shown to be associated with obesity and type 2 diabetes in population of European and non-European ethnicity. However, studies in Indian population have provided inconsistent results. Here, we examined association of eight FTO variants (rs1421085, rs8050136, rs9939609, rs9930506, rs1861867, rs9926180, rs2540769 and rs708277) with obesity and type 2 diabetes in 5364 North Indians (2474 type 2 diabetes patients and 2890 non-diabetic controls) in two stages. None of the variants including previously reported intron 1 variants (rs1421085, rs8050136, rs9939609 and rs9930506) showed body mass index (BMI)-dependent/independent association with type 2 diabetes. However, rs1421085, rs8050136 and rs9939609 were associated with obesity status and measures of obesity (BMI, waist circumference and waist-to-hip ratio) in stage 2 and combined study population. Meta-analysis of the two study population results also revealed that rs1421085, rs8050136 and rs9939609 were significantly associated with BMI both under the random- and fixed-effect models ( P (random/fixed)=0.02/0.0001, 0.004/0.0006 and 0.01/0.01, respectively). In conclusion, common variants of FTO were associated with obesity, but not with type 2 diabetes in North Indian population.

Insulin resistance (IR) and type 2 diabetes mellitus (T2DM) have been found to be associated with postprandial hypertriglyceridemia (PPHTg). However, whether PPHTg can cause IR and diabetes is not clear. We therefore investigated the role of PPHTg in development of T2DM in rat model of T2DM. 96 male Wistar rats were randomized into four groups (24 rats each). Control Group A, high sucrose diet (HSD) Group B, HSD+Pioglitazone (10 mg/kg/day) Group C and HSD+Atorvastatin (20 mg/kg/day) Group D. Fat and glucose tolerance tests were done at regular intervals in all groups besides insulin and body weight measurement. At 26 weeks, low dose streptozotocin (15 mg/kg, i.p.) was given to half of the rats. All rats were followed up till 48 weeks. PPHTg developed as early as week 2 in Group B and stabilized by week 14. Group B displayed highest PPHTg compared to other groups. Atorvastatin treatment (Group D) abolished PPHTg which became comparable to controls, pioglitazone treatment partially blunted PPHTg resulting in intermediate PPHTg. Group B with highest PPHTg showed highest subsequent IR, glucose intolerance (GI) and highest incidence of prediabetes at week 26 and diabetes at week 34 and 46 compared to other groups. Group D rats displayed lower IR, GI, low incidence of prediabetes and diabetes at these time points compared to Groups B and C. ROC analysis showed that triglyceride area under the curve of each time point significantly predicts the risk of diabetes. Present study provides the evidence that PPHTg predicts the development of IR, GI and T2DM in rat model of diet induced T2DM.

Indians undergoing socioeconomic and lifestyle transitions will be maximally affected by epidemic of type 2 diabetes (T2D). We conducted a two-stage genome-wide association study of T2D in 12,535 Indians, a less explored but high-risk group. We identified a new type 2 diabetes–associated locus at 2q21, with the lead signal being rs6723108 (odds ratio 1.31; P = 3.32 × 10−9). Imputation analysis refined the signal to rs998451 (odds ratio 1.56; P = 6.3 × 10−12) within TMEM163 that encodes a probable vesicular transporter in nerve terminals. TMEM163 variants also showed association with decreased fasting plasma insulin and homeostatic model assessment of insulin resistance, indicating a plausible effect through impaired insulin secretion. The 2q21 region also harbors RAB3GAP1 and ACMSD; those are involved in neurologic disorders. Forty-nine of 56 previously reported signals showed consistency in direction with similar effect sizes in Indians and previous studies, and 25 of them were also associated (P < 0.05). Known loci and the newly identified 2q21 locus altogether explained 7.65% variance in the risk of T2D in Indians. Our study suggests that common susceptibility variants for T2D are largely the same across populations, but also reveals a population-specific locus and provides further insights into genetic architecture and etiology of T2D.

Background: Organochlorine pesticides (OCPs) exposure may induce an endocrine disruption which may lead to the risk of developing diabetes through alteration and disturbance of glucose metabolism, insulin resistance, and destruction of β-cells. The present study determines the recent trend of OCPs residue in blood samples and their association with the known risk factors responsible for developing the risk of diabetes among the North Indian population.Methods: Blood sample of 300 patients (100 each of normal glucose tolerance [NGT], prediabetes and newly detected diabetes mellitus [DM]) between the age group of 30 to 70 years were collected. OCPs residue in whole blood samples was analyzed by using gas chromatography equipped with a 63Ni selective electron capture detector.Results: Significantly higher levels of β-hexachlorocyclohexane (HCH), dieldrin, and p,p’-dichloro-diphenyl-dichloroethylene (DDE) were found in the prediabetes and newly detected DM groups as compared to NGT group. Insulin resistance showed to be significantly positive correlation with β-HCH and dieldrin. Also, fasting and postprandial glucose levels were significantly positively correlated with levels of β-HCH, dieldrin, and p,p’-DDE. Further, when OCPs level was adjusted for age and body mass index (BMI), it was found that β-HCH, dieldrin, and p,p’-DDE levels in blood increases the risk of diabetes by 2.70, 2.83, and 2.55 times respectively. Moreover, when we adjust OCPs level based on BMI categories (BMI <23, ≥23, and ≤25, and >25 kg/m2); β-HCH and p,p’-DDE showed a significant risk of developing newly detected DM with BMI >25 and ≥23 and ≤25 kg/m2.Conclusion: The OCPs level present in the environment may be responsible for biological, metabolic, and endocrine disruptions within the human body which may increase the risk of developing newly detected DM. Hence, OCPs exposure can play a crucial role in the etiology of diabetes.

Background: Exposure to dichlorodiphenyltrichloroethane (DDT), a potent lipophilic organochlorine pesticide, has long been linked as a risk factor for type 2 diabetes mellitus (T2DM). However, its presence in the adipose tissues of the T2DM subjects has not been explored in the Indian population, where this long-banned pesticide is still in use. The present study was conducted to evaluate the possible association of DDT and its metabolites in obese and non-obese T2DM subjects. Methods: Subjects with normal glucose tolerance (n = 50) and T2DM (n = 50) were divided into equal numbers in obese and non-obese groups. Their plasma glucose levels, HbA1c, and lipid profile were measured. The adipose tissues were collected intraoperatively, and DDT and its metabolites were measured using a gas chromatograph equipped with an electron capture detector. Results: Obese subjects, irrespective of their glycemic status, and T2DM subjects had higher concentrations of DDT. p, p′ DDT was found to increase the odds for diabetes, and o, p′ DDT for central obesity. p, p′ DDD was also strongly correlated with central obesity, glycemic parameters, and triglycerides. Conclusion: The excess deposition of p, p′ DDD, o, p′ DDT, and p, p′ DDT in obese subjects may proceed to T2DM by disrupting triglycerides and glycemic parameters.

Indians, a rapidly growing population, constitute vast genetic heterogeneity to that of Western population; however they have become a sedentary population in past decades due to rapid urbanization ensuing in the amplified prevalence of metabolic syndrome (MetS). We performed a genome-wide association study (GWAS) of MetS in 10,093 Indian individuals (6617 MetS and 3476 controls) of Indo-European origin, that belong to our previous biorepository of The Indian Diabetes Consortium (INDICO). The study was conducted in two stages—discovery phase (N = 2158) and replication phase (N = 7935). We discovered two variants within/near the CETP gene—rs1800775 and rs3816117—associated with MetS at genome-wide significance level during replication phase in Indians. Additional CETP loci rs7205804, rs1532624, rs3764261, rs247617, and rs173539 also cropped up as modest signals in Indians. Haplotype association analysis revealed GCCCAGC as the strongest haplotype within the CETP locus constituting all seven CETP signals. In combined analysis, we perceived a novel and functionally relevant sub-GWAS significant locus—rs16890462 in the vicinity of SFRP1 gene. Overlaying gene regulatory data from ENCODE database revealed that single nucleotide polymorphism (SNP) rs16890462 resides in repressive chromatin in human subcutaneous adipose tissue as characterized by the enrichment of H3K27me3 and CTCF marks (repressive gene marks) and diminished H3K36me3 marks (activation gene marks). The variant displayed active DNA methylation marks in adipose tissue, suggesting its likely regulatory activity. Further, the variant also disrupts a potential binding site of a key transcription factor, NRF2, which is known for involvement in obesity and metabolic syndrome.

Overweight and obesity are rapidly increasing in countries like India. This study was aimed at determining the prevalence of generalized, abdominal and combined obesity in urban and rural India. Phase I of the ICMR-INDIAB study was conducted in a representative population of three States [Tamil Nadu (TN), Maharashtra (MH) and Jharkhand (JH)] and one Union Territory (UT)[Chandigarh (CH)] of India. A stratified multi-stage sampling design was adopted and individuals ≥ 20 yr of age were included. WHO Asia Pacific guidelines were used to define overweight [body mass index (BMI) ≥ 23 kg/m [2] but < 25 kg/m [2]], generalized obesity (GO, BMI ≥ 25 kg/m [2], abdominal obesity (AO, waist circumference ≥ 90 cm for men and ≥ 80 cm for women) and combined obesity (CO, GO plus AO). Of the 14,277 participants, 13,800 subjects (response rate, 96.7%) were included for the analysis (urban: n = 4,063; rural: n = 9737). The prevalence of GO was 24.6, 16.6, 11.8 and 31.3 per cent among residents of TN, MH, JH and CH, while the prevalence of AO was 26.6, 18.7, 16.9 and 36.1 per cent, respectively. CO was present in 19.3, 13.0, 9.8 and 26.6 per cent of the TN, MH, JH and CH population. The prevalence of GO, AO and CO were significantly higher among urban residents compared to rural residents in all the four regions studied. The prevalence of overweight was 15.2, 11.3, 7.8 and 15.9 per cent among residents of TN, MH, JH and CH, respectively. Multiple logistic regression analysis showed that female gender, hypertension, diabetes, higher socio-economic status, physical inactivity and urban residence were significantly associated with GO, AO and CO in all the four regions studied. Age was significantly associated with AO and CO, but not with GO. Prevalence of AO as well as of GO were high in India. Extrapolated to the whole country, 135, 153 and 107 million individuals will have GO, AO and CO, respectively. However, these figures have been estimated from three States and one UT of India and the results may be viewed in this light.

We aimed to compare the efficacy of daily v. low dose depot oral vitamin D3 for treating nutritional rickets. We conducted a randomised controlled trial in the department of paediatrics of a tertiary care hospital catering to semi-urban and rural population in Delhi, India. We randomised sixty-six children aged 3 months to 5 years with nutritional rickets to receive either daily oral vitamin D3 drops (3–12 months: 2000 IU; > 12 months to 5 years: 4000 IU; n 33) for 12 weeks duration or a single oral depot dose of vitamin D3 granules (3–12 months: 60 000 IU; > 12 months to 5 years: 150 000 IU; n 33). Participants in both groups had comparable demographic characteristics, laboratory features and radiological severity of rickets. Thirty-three participants in each group received the assigned intervention and all were followed up till 12 weeks. At 12 weeks follow-up, children in both groups showed a significant improvement in all biochemical parameters (serum Ca, P, alkaline phosphatase (ALP), parathormone and 25(OH) vitamin D levels) as well as radiological healing. At 12 weeks, the mean serum 25(OH) vitamin D levels (nmol/l) were statistically comparable in both groups (daily: 120·2 (sd 83·2), depot: 108 (sd 74), P = 0·43) and 31 (93·9 %) children in each group had radiological healing (Thacher score < 1·5). Two children in each group persisted to have raised ALP, and one child each in the daily group continued to have hypocalcaemia and hypophosphataemia at 12 weeks. Low dose oral depot vitamin D3 is an effective alternative to daily oral vitamin D3 for nutritional rickets.

We aimed to compare the efficacy of daily v . low dose depot oral vitamin D 3 for treating nutritional rickets. We conducted a randomised controlled trial in the department of paediatrics of a tertiary care hospital catering to semi-urban and rural population in Delhi, India. We randomised sixty-six children aged 3 months to 5 years with nutritional rickets to receive either daily oral vitamin D 3 drops (3–12 months: 2000 IU; > 12 months to 5 years: 4000 IU; n 33) for 12 weeks duration or a single oral depot dose of vitamin D 3 granules (3–12 months: 60 000 IU; > 12 months to 5 years: 150 000 IU; n 33). Participants in both groups had comparable demographic characteristics, laboratory features and radiological severity of rickets. Thirty-three participants in each group received the assigned intervention and all were followed up till 12 weeks. At 12 weeks follow-up, children in both groups showed a significant improvement in all biochemical parameters (serum Ca, P, alkaline phosphatase (ALP), parathormone and 25(OH) vitamin D levels) as well as radiological healing. At 12 weeks, the mean serum 25(OH) vitamin D levels (nmol/l) were statistically comparable in both groups (daily: 120·2 ( sd 83·2), depot: 108 ( sd 74), P = 0·43) and 31 (93·9 %) children in each group had radiological healing (Thacher score < 1·5). Two children in each group persisted to have raised ALP, and one child each in the daily group continued to have hypocalcaemia and hypophosphataemia at 12 weeks. Low dose oral depot vitamin D 3 is an effective alternative to daily oral vitamin D 3 for nutritional rickets.