Gokulakrishnan Kuppan

Publications (2)4.95 Total impact

• Source

  Available from: Sathishkumar Chandrakumar

  Article: Inflammatory markers in relation to nonalcoholic fatty liver disease in urban South Indians.

  Gokulakrishnan Kuppan, Ranjit Mohan Anjana, Mohan Deepa, Prabu Paramasivam, Sathishkumar Chandrakumar, Velmurugan Kaliyaperumal, Viswanathan Mohan
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  ABSTRACT: This study assessed the association of inflammatory markers, high-sensitivity C-reactive protein (hsCRP), and total leukocyte count with nonalcoholic fatty liver disease (NAFLD) in urban South Indians. We randomly selected subjects with and without NAFLD (n=100 each) from the Chennai Urban Rural Epidemiology Study conducted in Chennai in south India. NAFLD was diagnosed by ultrasonography. hsCRP was measured by nephelometry, and leukocyte count was measured by flow cytometry. Insulin resistance was analyzed by homeostasis assessment model using the following expression: fasting insulin (μIU/mL)×fasting glucose (mmol/L)/22.5. Mean hsCRP values were significantly higher in subjects with NAFLD compared with those without (4.2±1.2 mg/L vs. 2.2±0.4 mg/L; P<0.001). Leukocyte count was also higher in subjects with NAFLD compared with those without (7.8±1.4×10(3)/μL vs 6.9±0.9×10(3)/μL, P<0.001). Both hsCRP (P<0.001) and leukocyte count (P<0.001) increased with increasing severity of NAFLD. Multiple logistic regression analysis was done using NAFLD as the dependent variable and hsCRP and leukocyte count as independent variables. Both hsCRP (odds ratio 1.293, 95% confidence interval 1.13-1.470, P<0.001) and leukocyte count (odds ratio 1.293, 95% confidence interval 1.069-1.564, P=0.008) had a significant association with NAFLD even after adjusting for waist circumference, insulin resistance, serum triglycerides, and presence of type 2 diabetes. hsCRP and leukocyte count are associated with NAFLD after adjusting for conventional cardiometabolic risk factors.
  Diabetes Technology &amp Therapeutics 12/2011; 14(2):152-8. · 1.93 Impact Factor
• Article: Transcriptional regulation of cytokines and oxidative stress by gallic acid in human THP-1 monocytes.

  Gokulakrishnan Kuppan, Jayashree Balasubramanyam, Finny Monickaraj, Gayatri Srinivasan, Viswanathan Mohan, Muthuswamy Balasubramanyam
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  ABSTRACT: Increased inflammation/prooxidation has been linked not only to Type 2 diabetes but also in prediabetes state. In this study we investigated hyperglycemia-mediated proinflammatory/prooxidant effects in THP-1 monocytes and tested whether gallic acid could attenuate changes in gene expression induced by high-glucose. Cells were treated either with 5.5mM glucose or 25mM glucose in the absence and presence of gallic acid. While oxidative DNA damage was assessed by COMET assay, GSH and GSSG levels were estimated fluorimetrically. Gene expression patterns were determined by RT-PCR. Cells treated with high-glucose showed increased DNA damage and glutathione depletion and this was attenuated in the presence of gallic acid. High-glucose treated cells exhibited increased mRNA expression of TNF-alpha, IL-6, NADPH oxidase and TXNIP and gallic acid attenuated these proinflammatory and prooxidant effects. Cells treated with high-glucose revealed a deficiency in mounting SOCS-3 expression and gallic acid upregulates this feedback regulatory signal. Gallic acid attenuates DNA damage, maintains glutathione turnover, and suppresses hyperglycemia-induced activation of proinflammatory and prooxidant gene expression. Gallic acid beneficially modulate transcription of functionally diverse groups of genes and its regulation of SOCS-3 and TXNIP signals is a newly identified mechanism that has therapeutic implications.
  Cytokine 12/2009; 49(2):229-34. · 3.02 Impact Factor