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

Taher M, Mohamed Amiroudine MZ, Tengku Zakaria TM, Susanti D, Ichwan SJ, Kaderi MA, Ahmed QU, Zakaria ZA - Evid Based Complement Alternat Med (2015)

Bottom Line: 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-[(3)H] glucose uptake activity showed that α-mangostin significantly improved the glucose uptake (P < 0.05) with highest activity found at 25 μM.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmaceutical Technology, Faculty of Pharmacy, International Islamic University Malaysia, Jalan Istana, Bandar Indera Mahkota, 25200 Kuantan, Pahang, Malaysia.

ABSTRACT
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-[(3)H] 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.

No MeSH data available.


Related in: MedlinePlus

Glycerol release of different concentration of α-mangostin (10, 25, 50 μM) from the 3T3-L1 cells. Data is represented as mean ± SD, with n = 3 per group. *P < 0.05 compared to control group (DMSO treated cells).
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fig5: Glycerol release of different concentration of α-mangostin (10, 25, 50 μM) from the 3T3-L1 cells. Data is represented as mean ± SD, with n = 3 per group. *P < 0.05 compared to control group (DMSO treated cells).

Mentions: Figure 5 shows that the adipolysis assay served as confirmatory results for the adipogenesis assay. The amount of glycerol released into the medium was proportional to the level of triglyceride storage and degree of adipolysis. It was found that cells treated with α-mangostin increased the amount of free fatty acid released into the medium. It was further observed that the α-mangostin result was similar with the isoproterenol (10 μM), which was used as the positive control for the study. Lipolysis was measured by quantifying the glycerol released into the medium. Lipolysis in adipocytes is modulated in a stepwise fashion by several genes including the leptin. After this gene initiates the lipolysis pathway by releasing the fatty acids, glycerols are also released [51]. Moreover, it has been reported that plant extracts that inhibit the adipocyte differentiation of 3T3-L1 cells will also decrease the serum triglyceride levels in the adipose tissue [52]. These evidences show that decreased adipocytes differentiation may trigger the adipocytes to release the triglyceride into the medium.


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

Taher M, Mohamed Amiroudine MZ, Tengku Zakaria TM, Susanti D, Ichwan SJ, Kaderi MA, Ahmed QU, Zakaria ZA - Evid Based Complement Alternat Med (2015)

Glycerol release of different concentration of α-mangostin (10, 25, 50 μM) from the 3T3-L1 cells. Data is represented as mean ± SD, with n = 3 per group. *P < 0.05 compared to control group (DMSO treated cells).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4385643&req=5

fig5: Glycerol release of different concentration of α-mangostin (10, 25, 50 μM) from the 3T3-L1 cells. Data is represented as mean ± SD, with n = 3 per group. *P < 0.05 compared to control group (DMSO treated cells).
Mentions: Figure 5 shows that the adipolysis assay served as confirmatory results for the adipogenesis assay. The amount of glycerol released into the medium was proportional to the level of triglyceride storage and degree of adipolysis. It was found that cells treated with α-mangostin increased the amount of free fatty acid released into the medium. It was further observed that the α-mangostin result was similar with the isoproterenol (10 μM), which was used as the positive control for the study. Lipolysis was measured by quantifying the glycerol released into the medium. Lipolysis in adipocytes is modulated in a stepwise fashion by several genes including the leptin. After this gene initiates the lipolysis pathway by releasing the fatty acids, glycerols are also released [51]. Moreover, it has been reported that plant extracts that inhibit the adipocyte differentiation of 3T3-L1 cells will also decrease the serum triglyceride levels in the adipose tissue [52]. These evidences show that decreased adipocytes differentiation may trigger the adipocytes to release the triglyceride into the medium.

Bottom Line: 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-[(3)H] glucose uptake activity showed that α-mangostin significantly improved the glucose uptake (P < 0.05) with highest activity found at 25 μM.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmaceutical Technology, Faculty of Pharmacy, International Islamic University Malaysia, Jalan Istana, Bandar Indera Mahkota, 25200 Kuantan, Pahang, Malaysia.

ABSTRACT
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-[(3)H] 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.

No MeSH data available.


Related in: MedlinePlus