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Articles by S Ghosh
Total Records ( 3 ) for S Ghosh
  P Tantiwong , K Shanmugasundaram , A Monroy , S Ghosh , M Li , R. A DeFronzo , E Cersosimo , A Sriwijitkamol , S Mohan and N. Musi
 

NF-B is a transcription factor that controls the gene expression of several proinflammatory proteins. Cell culture and animal studies have implicated increased NF-B activity in the pathogenesis of insulin resistance and muscle atrophy. However, it is unclear whether insulin-resistant human subjects have abnormal NF-B activity in muscle. The effect that exercise has on NF-B activity/signaling also is not clear. We measured NF-B DNA-binding activity and the mRNA level of putative NF-B-regulated myokines interleukin (IL)-6 and monocyte chemotactic protein-1 (MCP-1) in muscle samples from T2DM, obese, and lean subjects immediately before, during (40 min), and after (210 min) a bout of moderate-intensity cycle exercise. At baseline, NF-B activity was elevated 2.1- and 2.7-fold in obese nondiabetic and T2DM subjects, respectively. NF-B activity was increased significantly at 210 min following exercise in lean (1.9-fold) and obese (2.6-fold) subjects, but NF-B activity did not change in T2DM. Exercise increased MCP-1 mRNA levels significantly in the three groups, whereas IL-6 gene expression increased significantly only in lean and obese subjects. MCP-1 and IL-6 gene expression peaked at the 40-min exercise time point. We conclude that insulin-resistant subjects have increased basal NF-B activity in muscle. Acute exercise stimulates NF-B in muscle from nondiabetic subjects. In T2DM subjects, exercise had no effect on NF-B activity, which could be explained by the already elevated NF-B activity at baseline. Exercise-induced MCP-1 and IL-6 gene expression precedes increases in NF-B activity, suggesting that other factors promote gene expression of these cytokines during exercise.

  J Kumar , G Garg , A Kumar , E Sundaramoorthy , K. R Sanapala , S Ghosh , G Karthikeyan , L Ramakrishnan and Sengupta Indian Genome Variation Consortium
 

Background— An elevated level of homocysteine (hyperhomocysteinemia) has been implicated as an independent risk factor for cardiovascular diseases. Deficiency of dietary factors like vitamin B12, folate, and genetic variations can cause hyperhomocysteinemia. The prevalence of hyperhomocysteinemia in the Indian population is likely to be high because most Indians adhere to a vegetarian diet, deficient in vitamin B12. In the background of vitamin B12 deficiency, variations in genes involved in homocysteine metabolism might have a greater impact on homocysteine levels.

Methods and Results— We genotyped 44 nonsynonymous single-nucleotide polymorphisms (nsSNPs) from 11 genes involved in homocysteine metabolism and found only 14 to be polymorphic. These 14 nsSNPs were genotyped in 546 individuals recruited from a tertiary care center in New Delhi, India, and it was found that choline dehydrogenase (CHDH A119C) and methylenetetrahydrofolate reductase (MTHFR C677T) were significantly associated with plasma total homocysteine levels (P=0.009 and P=0.001, respectively). These 2 SNPs were further genotyped in 330 individuals recruited from the same center, and the association remained significant even after increasing the sample size. Furthermore, we found the possibility of a significant interaction between vegetarian diet and the 2 polymorphisms that could explain the variation of homocysteine levels. We also genotyped all the polymorphic nsSNPs in apparently healthy individuals recruited from 24 different subpopulations (based on their linguistic lineage) spread across the country to determine their basal frequencies. The frequencies of these SNPs varied significantly between linguistic groups.

Conclusion— Vegetarian diet along with CHDH A119C and MTHFR C677T play an important role in modulating the homocysteine levels in Indian population.

  J Petremand , N Bulat , A. C Butty , C Poussin , S Rutti , K Au , S Ghosh , V Mooser , B Thorens , J. Y Yang , C Widmann and G. Waeber
 

High-density lipoproteins (HDLs) protect pancreatic β-cells against apoptosis. This property might relate to the increased risk to develop diabetes in patients with low HDL blood levels. However, the mechanisms by which HDLs protect β-cells are poorly characterized. Here we used a transcriptomic approach to identify genes differentially modulated by HDLs in β-cells subjected to apoptotic stimuli. The transcript encoding 4E-binding protein (4E-BP)1 was up-regulated by serum starvation, and HDLs blocked this increase. 4E-BP1 inhibits cap-dependent translation in its non- or hypophosphorylated state but it loses this ability when hyperphosphorylated. At the protein level, 4E-BP1 was also up-regulated in response to starvation and IL-1β, and this was blunted by HDLs. Whereas an ectopic increase of 4E-BP1 expression induced β-cell death, silencing 4E-BP1 increase with short hairpin RNAs inhibited the apoptotic-inducing capacities of starvation. HDLs can therefore protect β-cells by blocking 4E-BP1 protein expression, but this is not the sole protective mechanism activated by HDLs. Indeed, HDLs blocked apoptosis induced by endoplasmic reticulum stress with no associated decrease in total 4E-BP1 induction. Although, HDLs favored the phosphorylation, and hence the inactivation of 4E-BP1 in these conditions, this appeared not to be required for HDL protection. Our results indicate that HDLs can protect β-cells through modulation of 4E-BP1 depending on the type of stress stimuli.

 
 
 
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