Metformin attenuates inflammation and improves insulin sensitivity in coculture of LPS-induced 3T3-L1 adipocytes and RAW 264.7 macrophages mediated by IRS-1/GLUT-4 pathway.
Siska Andrina Kusumastuti, Dwi Aris Agung Nugrahaningsih, Mae Sri Hartati Wahyuningsih
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引用次数: 0
Abstract
Objective: Metformin is an anti-diabetic drug used to control blood glucose levels. The effects of metformin on insulin sensitivity in inflammation-induced adipocytes are not fully understood.This study aimed to explore the mechanism of metformin on insulin sensitivity enhancement in the coculture of LPS-induced 3T3-L1 adipocytes and RAW 264.7 macrophages.
Material and methods: Insulin resistance was induced in coculture cells using Lipopolysaccharide, followed by adding 25, 50, and 100 µg/ml of metformin for 24 h of incubation. Glucose consumption, GLUT-4, IRS-1, and IL-6 mRNA expressions were quantified.
Results: Metformin, starting at a concentration of 25 µg/ml, enhanced glucose consumption, upregulated GLUT-4 mRNA expression, and stimulated the expression of IRS-1 mRNA in coculture cells at 100 µg/ml of concentration. Additionally, Metformin inhibited inflammation by reducing IL-6 mRNA expression in coculture cells up to 100 µg/ml.
Discussion and conclusion: These findings suggest that metformin attenuated inflammation and improved insulin sensitivity in inflammation-induced adipocytes that may be mediated by the IRS-1/GLUT-4 pathway.
期刊介绍:
Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders.
The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications.
Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics:
-Dysregulation of hormone receptors and signal transduction
-Contribution of gene variants and gene regulatory processes
-Impairment of intermediary metabolism at the cellular level
-Secretion and metabolism of peptides and other factors that mediate cellular crosstalk
-Therapeutic strategies for managing metabolic diseases
Special issues dedicated to topics in the field will be published regularly.