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.

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.