Dr. Kirubhanand C is an Associate Professor in the Department of Anatomy at AIIMS Nagpur, Maharashtra. He holds a B.Sc. in Zoology (University of Madras, 2006), an M.Sc. in Anatomy (University of Madras, 2009), and a Ph.D. in Neuroscience and Stem Cell Biology (University of Madras, 2014). His doctoral research focused on the effect of autologous bone marrow stem cells in treating spinal cord injuries.
With extensive academic and research experience, Dr. Kirubhanand has served in various teaching positions, including Assistant Professor at Karuna Medical College and AIIMS Nagpur before being promoted to Associate Professor in 2022. He has received multiple awards, including the DST-INSPIRE Fellowship (2010), Young Researcher Award (2021), and Outstanding Researcher in Anatomy (2023).
Dr. Kirubhanand has published extensively in SCI-indexed journals, covering areas such as stem cell research, neuroscience, molecular docking, and bioinformatics. His contributions to medical science, along with his involvement in academic excellence, make him a distinguished figure in the field of anatomy and medical research.
Neuroscience, Stem Cell Biology, Molecular Docking, Bioinformatics, and Regenerative Medicine.
β-Sitosterol Circumvents Obesity-Induced Insulin Resistance by Down-Regulating Molecular Signaling Pathway in Adipocytes of Type 2 Diabetic Rats
β-Sitosterol (SIT), the most abundant bioactive component of vegetable oils and other plants, is a highly potent antidiabetic agent. Previous studies have shown that SIT controls hyperglycemia and insulin resistance by activating insulin receptors and glucose transporter 4 (GLUT-4) in the adipocytes of obesity-induced type 2 diabetic rats. The current study investigates whether SIT can exert its antidiabetic effects by mitigating adipocyte-induced inflammation, a key factor contributing to insulin resistance in obese individuals.
An effective dose of SIT (20 mg/kg body weight) was administered orally for 30 days to high-fat diet and sucrose-induced type 2 diabetic rats. Metformin, a conventionally used antidiabetic drug, was used as a positive control.
Our results indicate that SIT treatment restores the elevated serum levels of pro-inflammatory cytokines, including leptin, resistin, tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6), to normal levels while increasing anti-inflammatory adipocytokines such as adiponectin in type 2 diabetic rats. SIT decreases the expression of sterol regulatory element-binding protein-1c (SREBP-1c) and enhances peroxisome proliferator-activated receptor-γ (PPAR-γ) gene expression in adipocytes of diabetic rats. Furthermore, SIT acts as effectively as metformin in mitigating inflammation and insulin resistance in diabetic rats. Our findings demonstrate that SIT inhibits obesity-induced insulin resistance by ameliorating inflammatory events in adipose tissue through the downregulation of the IKKβ/NF-κB and c-Jun N-terminal kinase (JNK) signaling pathways.
References
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Scheja, L.; Heeren, J. The endocrine function of adipose tissues in health and cardiometabolic disease. Nat. Rev. Endocrinol. 2019, 15, 507–524.