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Debasish Roy

Researcher at VIT University

Publications -  11
Citations -  305

Debasish Roy is an academic researcher from VIT University. The author has contributed to research in topics: Adipose tissue & Naringenin. The author has an hindex of 8, co-authored 11 publications receiving 217 citations. Previous affiliations of Debasish Roy include Ohio State University & Boston University.

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Naringenin inhibits α-glucosidase activity: A promising strategy for the regulation of postprandial hyperglycemia in high fat diet fed streptozotocin induced diabetic rats

TL;DR: It is suggested that naringenin exerts significant inhibition of intestinal α-glucosidase activity in vivo thereby delaying the absorption of carbohydrates in T2D rats, thus resulting in significant lowering of postprandial blood glucose levels.
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Chenodeoxycholic acid, an endogenous FXR ligand alters adipokines and reverses insulin resistance.

TL;DR: The altered adipokines in insulin resistance, its association with inflammatory regulators, and the role of CDCA in amelioration of insulin resistance by modulation of adipokine secretion are shown.
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A rapid method to assess reactive oxygen species in yeast using H2DCF-DA

TL;DR: A protocol to efficiently assess Reactive Oxygen Species (ROS) levels in yeast cells using H2DCF-DA is described here, which obviates the need for both physical and enzymatic lysis methods that are arduous and time consuming.
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Evidence that Chemical Chaperone 4-Phenylbutyric Acid Binds to Human Serum Albumin at Fatty Acid Binding Sites.

TL;DR: The results show that 4-PBA has high binding specificity to Sudlow Site II (Fatty acid binding site 3, subdomain IIIA) and the binding constant as calculated from fluorescence spectroscopic studies was found to be kPBA = 2.69 x 105 M-1.
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Coordinated transcriptional control of adipocyte triglyceride lipase (Atgl) by transcription factors Sp1 and peroxisome proliferator-activated receptor γ (PPARγ) during adipocyte differentiation.

TL;DR: It is reported that Atgl is down-regulated by the basal transcription factor Sp1 in preadipocytes and that the magnitude of down-regulation depends on interactions between Sp1 and peroxisome proliferator–activated receptor γ (PPARγ).