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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

Effects of α-mangostin (25 μM) on leptin mRNA expression. 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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fig8: Effects of α-mangostin (25 μM) on leptin mRNA expression. Data is represented as mean ± SD, with n = 3 per group. *P < 0.05 compared to control group (DMSO treated cells).

Mentions: Finally, in the gene expression analysis, we evaluated the effect of α-mangostin on leptin expression to signify the free fatty acid release from the cells into the medium. Analysis with α-mangostin (25 μM) showed that the compound increased the leptin expression and the result was similar with insulin (100 nM) that was used as the positive control for the study (Figure 8). This result suggests that α-mangostin treatment may release the free fatty acid into the medium, which was confirmed by the leptin mRNA expression. In obese individuals, plasma leptin and free fatty acid are both elevated. Since free fatty acid also reduces plasma leptin levels in the in vitro study [5], it has been speculated that obesity may be caused by the abnormality in the leptin-reduction mechanism of free fatty acids. Alternatively, leptin resistance, which has been considered to be present in obesity, might overcome the decrease in leptin induced by free fatty acid [55].


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)

Effects of α-mangostin (25 μM) on leptin mRNA expression. 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

fig8: Effects of α-mangostin (25 μM) on leptin mRNA expression. Data is represented as mean ± SD, with n = 3 per group. *P < 0.05 compared to control group (DMSO treated cells).
Mentions: Finally, in the gene expression analysis, we evaluated the effect of α-mangostin on leptin expression to signify the free fatty acid release from the cells into the medium. Analysis with α-mangostin (25 μM) showed that the compound increased the leptin expression and the result was similar with insulin (100 nM) that was used as the positive control for the study (Figure 8). This result suggests that α-mangostin treatment may release the free fatty acid into the medium, which was confirmed by the leptin mRNA expression. In obese individuals, plasma leptin and free fatty acid are both elevated. Since free fatty acid also reduces plasma leptin levels in the in vitro study [5], it has been speculated that obesity may be caused by the abnormality in the leptin-reduction mechanism of free fatty acids. Alternatively, leptin resistance, which has been considered to be present in obesity, might overcome the decrease in leptin induced by free fatty acid [55].

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