Ameliorative Effect of Galic Acid in GLUT-4 Expression and Insulin Resistantance in High Fat Diet Induced Obesity Animal Model Mice, Mus musculus

Abstract

Abstract Objective - A primary loophole exacerbating the emergence of metabolic abnormalities is insulin resistance results due to impaired glucose transport. Glucose transporter type 4 isoform (GLUT-4) is a insulin-sensitive receptor associated with glucose uptake over the surface of adipocytes for glucose metabolism. Impaired insulin signalling is linked with reduced GLUT-4 activity. The aim of present study was to examine the expression of GLUT-4 and insulin receptor substrate-1 (IRS-1) in visceral adipose tissue of high fat diet induced (HFD) obesity animal model with respect to antidote gallic acid (GA). Methods - Experimental animal, female swiss albino mice were fed a standard and high-fat diet (HFD) in order to study the therapeutic effects of gallic acid (GA) against metabolic changes obesity induced HFD, animal model. Results - Experimental group fed HFD along with GA displayed improved triglyceride and serum cholesterol levels. Alongwith this hyperinsulinemia and an increase in homeostasis model assessment for insulin resistance (HOMA IR) were observed in HFD group, which were alleviated by GA. Apart from this, GA, had improved glucose tolerance test (GTT), and upregulation in mRNA expression of GLUT-4 and IRS-1 in visceral adipose tissues in HFD + GA experimental group. Conclusion - The current study found a link between insulin resistance, GLUT-4 and IRS-1 expression in adipose tissue and the beginning of the metabolic syndrome, a condition characterised by obesity. Gallic acid may enhance insulin signalling, glucose, and lipid metabolism in adipose tissues, and it may even be used to manage comorbidities related to obesity, such as diabetes type 2 and dyslipidemia.