| Literature DB >> 30461321 |
R Ponnulakshmi1, B Shyamaladevi2, P Vijayalakshmi3, J Selvaraj2.
Abstract
Adipose tissue is the primary site of storage for excess energy as triglyceride and it helps in synthesizing a number of biologically active compounds that regulate metabolic homeostasis. Consumption of high dietary fat increases stored fat mass and is considered as a main risk factor for metabolic diseases. Beta-sitosterol (β-sitosterol) is a plant sterol. It has the similar chemical structure like cholesterol. Clinical and experimental studies have shown that β-sitosterol has anti-diabetic, hypolipidemic, anti-cancer, anti-arthritic, and hepatoprotective role. However, effect of β-sitosterol on insulin signaling molecules and glucose oxidation has not been explored. Hence in the present study we aimed to discover the protective role of β-sitosterol on the expression of insulin signaling molecules in the adipose tissue of high-fat diet and sucrose-induced type-2 diabetic experimental rats. Effect dose of β-sitosterol (20 mg/kg b.wt, orally for 30 days) was given to high fat diet and sucrose-induced type-2 diabetic rats to study its anti-diabetic activity. Results of the study showed that the treatment with β-sitosterol to diabetes-induced rats normalized the altered levels of blood glucose, serum insulin and testosterone, lipid profile, oxidative stress markers, antioxidant enzymes, insulin receptor (IR), and glucose transporter 4 (GLUT4) proteins. Our present findings indicate that β-sitosterol improves glycemic control through activation of IR and GLUT4 in the adipose tissue of high fat and sucrose-induced type-2 diabetic rats. Insilico analysis also coincides with invivo results. Hence it is very clear that β-sitosterol can act as potent antidiabetic agent.Entities:
Keywords: adipose tissue; glucose uptake and oxidation; high-fat diet and sucrose; homology modeling; insulin signaling; molecular docking; molecular dynamics; type-2 diabetes; β-sitosterol
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Year: 2019 PMID: 30461321 DOI: 10.1080/15376516.2018.1545815
Source DB: PubMed Journal: Toxicol Mech Methods ISSN: 1537-6516 Impact factor: 2.987