Is the rural population of Puducherry district healthy in terms of the burden of non-communicable diseases? Findings from a cross-sectional analytical survey.

INTRODUCTION: Epidemiological transition remains a key contributor to the rising prevalence of non-communicable diseases (NCDs) across developing nations. Population-specific NCD risk factors estimates derived using World Health Organization (WHO) 'STEP-wise approach' are crucial for devising evidence-based public health interventions to combat NCDs. OBJECTIVE: To estimate the prevalence of behavioral and biological risk factors for NCDs among the rural adult population of Puducherry district in India. METHODOLOGY: STEPS survey was conducted by following all three steps (behavioral, physical measurements and biochemical risk factors) of NCD risk factor assessment. A total of 790 participants were selected from 50 villages through multistage cluster sampling method. STEPS instrument was used to assess behavioral risk factors, physical measurements and biochemical (fasting blood glucose and total cholesterol) risk factors. RESULTS: Tobacco use and alcohol consumption were present among 11.3% (95% Confidence Interval (CI): 9-13.6%) and 19.2% (95% CI: 16.5-22.4%) of the population, respectively. Low physical activity, inadequate intake of fruits and vegetables, overweight and obesity were observed among 29.3% (95% CI: 26.2-32.7%), 89.8% (95% CI: 87.6-92%), 15.6% (95% CI: 13.1-18.3%) and 38.9% (95% CI: 35.4-42.2%), respectively. About 28.2% (95% CI: 25.2-31.6%) had hypertension and 24.4% (95% CI: 20-29%) had diabetes mellitus. Abdominal obesity was twice highly prevalent among women. Tobacco and alcohol use were more common among men, whereas low physical activity, obesity and hypercholesterolemia were higher among women. CONCLUSION: Public health interventions to promote healthy lifestyle need to be initiated especially to increase physical activity, intake for fruits and vegetables, and quitting of tobacco and alcohol consumption in the rural population of Puducherry.

Amla prevents fructose-induced hepatic steatosis in ovariectomized rats: role of liver FXR and LXRα.

OBJECTIVES: Increased fructose consumption causes dyslipidemia and fatty liver in postmenopausal women, both independent risk factors for cardiovascular disease. This study explored the potential mechanisms by which amla (Emblica officinalis) reduced hypercholesterolemia and hypertriglyceridemia and prevented fatty liver in a fructose-fed, ovariectomized rat model of menopause. METHODS: Sham-operated and ovariectomized rats were put on a chow or high fructose diet. They were further divided into groups with or without amla. After 18 weeks of treatment, livers were harvested and subjected to Western blot and histological analyses. RESULTS: In all groups, amla increased the protein expression of liver farnesoid X receptor (FXR) and liver X receptor (LXR), key proteins involved in lipid metabolism. Fructose-fed rats developed fatty liver and amla prevented this. Here amla produced an exceptional rise in LXR and insulin-induced gene-2 (Insig-2) which prevented the maturation of sterol regulatory element-binding protein-1 and steroyl CoA desaturase-1, responsible for triglyceride synthesis. Amla also increased the protein expression of ATP binding cassette transporter A1 (ABCA1), involved in high density lipoprotein (HDL) synthesis as well as low density lipoprotein receptor (LDLR) responsible for uptake of LDL cholesterol. Besides this, amla increased the protein expression of peroxisome proliferator activated receptor α (PPARα) involved in ß oxidation of fatty acids. CONCLUSIONS: Amla increased the protein expression of liver FXR, LXRα, PPARα and their downstream proteins Insig-2, ABCA1 and LDLR. This property of amla to modulate some of the key proteins involved in lipid metabolism promises its usefulness as a preventive agent for dyslipidemia and hepatic steatosis.

Oxidative stress in severe dengue viral infection: association of thrombocytopenia with lipid peroxidation.

Oxidative stress in viral infections has been suggested. The study was carried out to assess the oxidative stress in the different clinical spectrums of dengue infection and to evaluate if thrombocytopenia is associated with lipid and protein oxidative injury. Twenty-seven dengue fever (DF), 32 dengue hemorrhagic fever (DHF) and 21 dengue shock syndrome (DSS) cases were studied at 3, 5 and 7 days of illness. Sixty-three healthy subjects were selected as controls. Serum protein carbonyls (PCOs), malendialdehyde (MDA) and total antioxidant status (TAS) were estimated in blood. Dengue infected individuals had significantly high levels of PCOs and MDA on the three days tested in comparison to controls. In DF cases, no significant changes in the levels of MDA and PCOs were found in course of time. However, among DHF and DSS, significant increase in MDA levels was found in the fifth and seventh day samples in comparison to their respective third day sample (P < 0.05). Using one way ANOVA, high PCOs levels were found in DSS in comparison to DF and DHF cases on all the three days tested (P < 0.001). TAS levels were found to be low among DSS on days 5 and 7 and day 7 in DHF when compared with DF cases. Correlation analysis between MDA and hematocrit revealed a significant positive association between them in DHF and DSS on day 5 (DHF r = 0.372; p = 0.024 and DSS r = 0.535; p = 0.0-01) and day 7 (DHF r = 0.412; p = 0.003 and DSS r = 0.765; p < 0.0001). There was an important negative correlation between platelet count and plasma lipid peroxidation levels among DHF and DSS on all three days tested [day 3 (DHF r = -0.392; p = 0.012 and DSS r = -0.453; p = 0.004), day 5 (DHF r = -0.592; p < 0.001 and DSS r = -0.581; p < 0.001) and day 7 (DHF r = -0.418; p = 0.001 and DSS r = -0.515; p = 0.002)]. This study concludes that an increase in oxidative stress was found in dengue viral infection. The level of oxidative stress was maximal in DSS followed by DHF and its severity was minimal in DF. The thrombocytopenia of dengue infection was associated with the extent of lipid peroxidation. Future studies might be carried out to find the role of oxidative damage in the ethiopathogenesis of thrombocytopenia and vascular leakage in dengue infection.

Association between protein bound sialic acid and high sensitivity C-reactive protein in prehypertension: a possible indication of underlying cardiovascular risk.

The global burden posed by cardiovascular disease due to a rising incidence of known risk factors like essential hypertension underlines an urgent need to identify other potential risk factors like dyslipidemia, elevated levels of high-sensitivity CRP (hsCRP), Apo-B, and sialic acid in prehypertensive subjects. This study sought to examine the possible alteration in the levels of hsCRP, plasma protein bound sialic acid, and other lipid risk factors and the possible interactions among these parameters in prehypertensive subjects. Forty prehypertensive and 34 normotensive male subjects were enrolled in the study. Lipid profile, hsCRP, Apo-B, sialic acid, and lipid risk ratios were estimated in both the groups. There was no significant difference between fasting glucose and BMI in either group. The levels of total cholesterol, triglycerides, direct LDL-cholesterol, non-HDL cholesterol, and Apo-B were significantly increased in prehypertensive subjects compared with controls. The risk ratios calculated as direct LDL-cholesterol/Apo-B, total cholesterol/HDL-cholesterol, non-HDL-cholesterol/HDL-cholesterol were significantly elevated in prehypertensive subjects. There was also a significant increase in hsCRP and protein bound sialic acid in prehypertensive subjects in comparison with normotensive subjects. Correlation analysis revealed a significant association between the protein bound sialic acid with hsCRP, LDL cholesterol, and LDL-C/Apo-B. The findings of the present study suggest that in prehypertension, there is an association between protein bound sialic acid and hsCRP that reflects the clustering of cardiovascular risk factors in these subjects.

Oxidative stress induced changes in plasma protein can be a predictor of imminent severe dengue infection.

OBJECTIVES: Oxidative stress in dengue viral infection has been suggested and severity of it was found to be associated with progress of illness. Hence assessing oxidative stress mediated changes in plasma proteins can be an early biomarker for prediction of severe dengue infection. DESIGN AND METHODS: Thirty two dengue hemorrhagic fever (DHF), 21 dengue shock syndrome (DSS), 27 dengue fever (DF) and 63 age and sex matched controls, were included in this study. Blood samples were collected on the 3rd day of fever. Protein carbonylation (PCOs) and protein-bound sulphydryl (PBSH) group levels were determined by spectrophotometric method and analyzed as predictor of dengue hemorrhagic fever and dengue shock syndrome. RESULTS: About 80-84% of cases presented with no signs of DHF/DSS at the time of sampling. Dengue infected individuals had significantly elevated PCOs and low PBSH group levels than the controls. Using one-way ANOVA we found a significant difference with high PCOs and low PBSH group levels between DHF and DSS when compared with DF (P<0.001). However, no difference was observed in PBSH group levels between DHF and DSS. A significant difference in PCOs to PBSH ratio was observed among DF, DHF and DSS (P<0.001). Linear regression analysis revealed that duration of hospitalization is dependent on PCOs and PBSH group levels. Receiver operator curve (ROC) analysis indicated that 5.22nmol/mg protein PCOs; 1.08 PCOs to PBSH group levels ratio were optimal cutoff value for predicting DHF with sensitivity and specificity of 87.5% and 74.1%; 96.9% and 81.5%, respectively. For DSS prediction, 6.13 nmol/mg protein PCOs; 1.16 PCOs to PBSH group levels ratio were found as effective cutoff with sensitivity and specificity of 81% and 71.9%; 95.2% and 56.2%, respectively. CONCLUSION: Oxidative stress has been observed to develop since early days of onset of dengue infection. Plasma PCOs, PCOs to PBSH group ratio were found to very well predict DHF/DSS.

Bitter gourd (Momordica charantia) improves insulin sensitivity by increasing skeletal muscle insulin-stimulated IRS-1 tyrosine phosphorylation in high-fat-fed rats.

The aim of this present study was to investigate the effect of bitter gourd extract on insulin sensitivity and proximal insulin signalling pathways in high-fat-fed rats. High-fat feeding of male Wistar rats for 10 weeks decreased the glucose tolerance and insulin sensitivity compared to chow-fed control rats. Bitter gourd extract supplementation for 2 weeks (9th and 10th) of high-fat feeding improved the glucose tolerance and insulin sensitivity. In addition bitter gourd extract reduced the fasting insulin (43 (se 4.4) v. 23 (se 5.2) microU/ml, P < 0.05), TAG (134 (se 12) v. 96 (se 5.5) mg/dl, P < 0.05), cholesterol (97 (se 6.3) v. 72 (se 5.2) mg/dl, P < 0.05) and epidydimal fat (4.8 (se 0.29) v. 3.6 (se 0.24) g, P < 0.05), which were increased by high-fat diet (HFD). High-fat feeding and bitter gourd supplementation did not have any effect on skeletal muscle insulin receptor, insulin receptor subtrate-1 (IRS-1) and insulin- stimulated insulin receptor tyrosine phosphorylation compared to chow-fed control rats. However high-fat feeding for 10 weeks reduced the insulin-stimulated IRS-1 tyrosine phosphorylation compared to control rats. Bitter gourd supplementation together with HFD for 2 weeks improved the insulin-stimulated IRS-1 tyrosine phosphorylation compared to rats fed with HFD alone. Our results show that bitter gourd extract improves insulin sensitivity, glucose tolerance and insulin signalling in HFD-induced insulin resistance. Identification of potential mechanism(s) by which bitter gourd improves insulin sensitivity and insulin signalling in high-fat-fed rats may open new therapeutic targets for the treatment of obesity/dyslipidemia-induced insulin resistance.

Oxidative stress: does it play a role in the genesis of early glycated proteins?

Glycation and oxidative stress are two important processes known to play a key role in complications of many pathophysiological processes. The two traditional factors found to modulate the early glycation of proteins are the prevailing concentration of glucose and half life of the protein. But evidences in the literature have documented an increased glycated protein levels in some non-diabetic pathological states. So it stands to reason that hyperglycemia, while clearly the culprit in diabetes, is not the complete answer to the etiology of increased early glycated products in non-diabetic conditions. A common denominator in all these above mentioned non-diabetic pathological conditions is oxidative stress. Collective evidences from the literature reveal that malondialdehyde, reduced glutathione, vitamin C, vitamin E and drugs with antioxidant properties mitigate the process of protein glycation. Taking all the above factors into account, we hypothesis that oxidative stress either via increasing reactive oxygen species or by depleting the antioxidants may modulate the genesis of early glycated proteins in vivo.

Increased plasma malondialdehyde and fructosamine in iron deficiency anemia: effect of treatment.

Glycation and lipid peroxidation are spontaneous reactions that are believed to play a key role in the pathogenesis of many clinical disorders. Glycation of proteins is enhanced by elevated glucose concentrations. However, increased glycated hemoglobin levels have been documented in iron deficiency anemic patients without any history of diabetes. Collective evidences reveal that lipid peroxidation can modulate protein glycation. This study was undertaken to unravel the possible association of malondialdehyde and fructosamine in iron deficient anemic patients and to observe the possible alteration in malondialdehyde and fructosamine levels in these patients after one month supplementation with iron. Twenty non-diabetic anemic patients and 16 age-matched healthy subjects were enrolled for this study. Plasma lipid peroxides, fasting glucose, fructosamine, iron, ferritin and hemoglobin were analyzed in both the groups. Partial correlation analysis was performed to predict the independent association of malondialdehyde and fasting glucose on fructosamine. In anemic patients, while fructosamine and malondialdehyde levels were found to be significantly increased, hemoglobin, iron and ferritin levels decreased significantly when compared to before treatment. Fructosamine was found to have a significant positive correlation with malondialdehyde even after nullifying the effect of glucose. After one month supplementation with iron, both fructosamine and malondialdehyde levels decreased significantly when compared to before treatment. There was a significant increase in iron, ferritin and hemoglobin levels in anemic patients after one month of treatment. In conclusion, an increased level of fructosamine and malondialdehyde was found in anemic patients. These data suggest that fructosamine levels are closely associated with malondialdehyde concentrations in iron deficient anemic patients.

Increased glycated hemoglobin level in non-diabetic nephrotic children is associated with oxidative stress.

Glycation and lipid peroxidation are spontaneous reactions believed to contribute to the pathogenesis of nephrotic syndrome. Possible interrelations of glycated hemoglobin with reduced glutathione and malondialdehyde were evaluated in nephrotic syndrome patients. Eighteen nephrotic syndrome patients and 15 healthy controls were enrolled for this study. Glycated hemoglobin, reduced glutathione, malondialdehyde and fasting glucose were analyzed for their correlation in both the groups. In nephrotic syndrome patients, while glycated hemoglobin and malondialdehyde levels were found to be significantly increased, glutathione levels decreased significantly when compared with controls. Glycated hemoglobin was found to have a significant positive correlation with malondialdehyde and a negative correlation with glutathione. Erythrocytes depleted of glutathione, by pre-treatment with 1-chloro-2, 4-dinitrobenezene, were found to have higher glycated hemoglobin levels when compared with erythrocytes incubated with glucose alone. These data suggest that glycated hemoglobin levels are closely associated with malondialdehyde and glutathione in nephrotic syndrome patients.

T-antigen (Gal ß3 GaINAc α-) containing glycoproteins of human reace.

Desialation of cell surface glycoconjugates due to bacterial or viral infection can expose epitopes like T-antigenic structure which can also occur during oncological transformations. Human platelet plasma membrane glycoproteins were isolated by jacalin affinity chromatography. Potential T-antigen containing glycoproteins which were not reported before could be identified on the Western blot using peanut agglutinin-horse radish peroxidase (PNA-HRP) after neuraminidase treatment. Alpha-galactosyl epitopes recognized by anti-gal were found to be absent in human platelet plasma membrane glycoproteins. Under the experimental conditions employed, the Gp IIbα was identified most rich in T-antigenic structures. Probable role of exposed T-antigenic structures and α-galactosyl epitopes in pathological conditions is discussed. The identity of major glycoprotein bands was confirmed by differential lectin-binding studies with Concanavalin A on the Western blot. The higher binding affinity of jacalin for T-antigenic structures when compared to PNA enabled the isolation and detection of the antigen containing platelet surface glycoproteins which were not reported before.