North Indian Type Research Articles

Inflammation, insulin resistance and carotid IMT in first degree relatives of north Indian type 2 diabetic subjects

Inflammation is associated with insulin resistance, atherosclerosis and type 2 diabetes but whether it causes insulin resistance and accelerated atherosclerosis or an epiphenomena of insulin resistance is not clear. Thirty-eight young normoglycemic, non-obese, first degree relatives of type 2 diabetic subjects (FH +) and 38 control subjects without family history of diabetes (FH −) (age and sex matched), were studied to determine difference in inflammatory markers, insulin resistance and carotid intima-media thickness (IMT). Plasma glucose, insulin (fasting and 2 h after 75 gm oral glucose) lipids and serum levels of C-reactive protein (CRP), tumour necrosis factor (TNF)-α and fibrinogen were measured after an overnight fast of 10–12 h. First degree relative group (FH +) have higher BMI ( p < 0.05), composite IMT ( p < 0.05) and CRP level ( p < 0.05), however, after adjustment for BMI, the two groups did not significantly differ. Fibrinogen was not significantly correlated with composite IMT in FH + group after controlling with BMI. In FH + group composite IMT was significantly correlated with systolic blood pressure ( p < 0.05), LDL-cholesterol ( p < 0.05), postprandial insulin level ( p < 0.05) and HOMA-IR ( p < 0.05) after adjustment of BMI. Thus insulin resistance is a major determinant of atherosclerosis in subjects with high risk of type 2 diabetes showing the strong relationship between inflammation, obesity and insulin resistance.

Postprandial hypertriglyceridemia and carotid intima–media thickness in north Indian type 2 diabetic subjects

Hypertriglyceridemia is an important risk factor for coronary heart disease (CHD) and in the development of atherosclerosis, especially in subgroups of the population like those with type 2 diabetes. Although triglycerides are generally increased in the postprandial period, the association between postprandial triglyceride (ppTG) levels and atherosclerosis has not been investigated in north Indian type 2 diabetic subjects known to have a very high prevalence rate of premature CHD and insulin resistance. To investigate the role of ppTG levels in atherosclerosis in type 2 diabetes, we examined the correlation between ppTG levels and carotid intima–media thickness (IMT). Carotid IMT was determined by high resolution B-mode ultrasonography in 86 newly detected type 2 diabetic subjects (1–12 months duration) having good glycemic control (HbA 1C < 7%) and 45 non-diabetic subjects matched according to age and body mass index (BMI). Plasma glucose, insulin, total cholesterol, LDL-cholesterol, HDL-cholesterol and triglycerides were measured after overnight fasting. Plasma insulin and glucose were also measured 2 h and plasma triglycerides 4 h after breakfast. The mean carotid IMT in diabetic subjects was higher than those in non-diabetic subjects (0.77 ± 0.15 mm versus 0.53 ± 0.16 mm, P < 0.001). Based on the fasting and postprandial triglyceride levels, the diabetic subjects were divided into three groups: normo–normo (NN); normo–hyper (NH); hyper–hyper (HH) [NN: fTG < 1.70 mmol/L and ppTG < 2.30 mmol/L; NH: fTG < 1.70 mmol/L and ppTG > 2.30 mmol/L; HH: fTG > 1.70 mmol/L and ppTG > 2.30 mmol/L]. Carotid IMT was significantly increased in the NH (0.79 ± 0.09 mm) and HH (0.82 ± 0.06 mm) groups compared with the NN group (0.59 ± 0.09 mm, P < 0.001). Although ppTG, age, fasting LDL-cholesterol, HOMA-estimated insulin resistance, HbA 1C were all independently correlated with carotid IMT, age and ppTG levels had the strongest statistical influence ( P < 0.002).

HLA and autoimmunity in North Indian type I (insulin-dependent) diabetic multiplex families.

The HLA haplotype segregation and autoantibody spectrum in 7 type I (insulin-dependent) diabetic multiplex families of North Indian origin were determined. Of the total of 17 diabetic sibs, 7 shared both haplotypes and 3 shared one haplotype with the proband. No HLA-non-identical sibs were observed. This distribution of haplotypes was non-random (P approximately equal to 0.005). The mode of inheritance was compatible with an autosomal recessive model, while a dominant model was unlikely. Pancreatic islet-cell antibodies were found in 23.5% of affected sibs, but in no healthy family member. A high incidence of other autoantibodies (parietal-cell and thyroglobulin/thyroid microsomal antibodies) was detected in both the diabetic patients (26.3%), and in healthy first-degree relatives (22.2%). These findings emphasize the role of HLA-linked genes and autoimmunity in the pathogenesis of type I diabetes in North India.

HLA-DR antigen frequencies in a North Indian type I diabetic population.

Eighty-eight North Indian patients with type I, insulin-dependent diabetes mellitus (IDDM) and 113 unaffected individuals were typed for HLA-DR antigens from DR1 to DR7. The frequency of HLA-DR3 was significantly increased in the patients as compared with the controls (78.4% versus 25.7%, corrected P = 1.68 X 10(-12], the relative risk (RR) of 10.52 being much higher than that reported in the Western IDDM population. HLA-DR2 showed a significant negative association (RR = 0.18, corrected P = 1.03 X 10(-5], but DR4 had no relationship with IDDM in the present study (RR = 1.12, P = 0.12). These results emphasize the differences in HLA-IDDM associations among different ethnic groups.

HLA-DR antigen frequencies in a North Indian type I diabetic population

HLA-DR antigen frequencies in a North Indian type I diabetic population