α-Mangostin Improves Glucose Uptake and Inhibits Adipocytes Differentiation in 3T3-L1 Cells via PPARγ, GLUT4, and Leptin Expressions

Abstract EN

Obesity has been often associated with the occurrence of cardiovascular diseases, type 2 diabetes, and cancer.

The development of obesity is also accompanied by significant differentiation of preadipocytes into adipocytes.

In this study, we investigated the activity of α-mangostin, a major xanthone component isolated from the stem bark of G.

malaccensis, on glucose uptake and adipocyte differentiation of 3T3-L1 cells focusing on PPARγ, GLUT4, and leptin expressions.

α-Mangostin was found to inhibit cytoplasmic lipid accumulation and adipogenic differentiation.

Cells treated with 50 μM of α-mangostin reduced intracellular fat accumulation dose-dependently up to 44.4% relative to MDI-treated cells.

Analyses of 2-deoxy-D-[3H] glucose uptake activity showed that α-mangostin significantly improved the glucose uptake ( P < 0.05 ) with highest activity found at 25 μM.

In addition, α-mangostin increased the amount of free fatty acids (FFA) released.

The highest glycerol release level was observed at 50 μM of α-mangostin.

qRT-PCR analysis showed reduced lipid accumulation via inhibition of PPARγ gene expression.

Induction of glucose uptake and free fatty acid release by α-mangostin were accompanied by increasing mRNA expression of GLUT4 and leptin.

These evidences propose that α-mangostin might be possible candidate for the effective management of obesity in future.