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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 PPARy 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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fig6: Effects of α-mangostin (25 μM) on PPARy mRNA expression. Data is represented as mean ± SD, with n = 3 per group. *P < 0.05 compared to control group (DMSO treated cells).

Mentions: To further assess the activity of α-mangostin on PPARγ  mRNA expression, 3T3-L1 preadipocytes were cultured with the indicated concentration of the compound (25 μM) in the presence of MDI. This method can evaluate the stimulation or inhibitory effect of the test compound on adipocyte differentiation. As shown in Figure 6, cells treated with α-mangostin showed reduced activity of PPARγ level when compared with the basal. Insulin (100 nM) was used as the positive control [53]. Increased expression of PPARγ induces adipocyte differentiation in 3T3-L1 cells whereas the suppression of PPARγ expression blocks the lipid formation [12]. In this study, analysis of the gene expression demonstrated that the 3T3-L1 cells treated with α-mangostin significantly downregulated the PPARγ  expression. Therefore, we can deduce that the reduction in PPARγmay be the key step in the inhibition of adipocyte differentiation [22] in 3T3-L1 and that the targeting of PPARγ could be the main mechanism for blocking of adipocyte differentiation by the α-mangostin.


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 PPARy 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

fig6: Effects of α-mangostin (25 μM) on PPARy mRNA expression. Data is represented as mean ± SD, with n = 3 per group. *P < 0.05 compared to control group (DMSO treated cells).
Mentions: To further assess the activity of α-mangostin on PPARγ  mRNA expression, 3T3-L1 preadipocytes were cultured with the indicated concentration of the compound (25 μM) in the presence of MDI. This method can evaluate the stimulation or inhibitory effect of the test compound on adipocyte differentiation. As shown in Figure 6, cells treated with α-mangostin showed reduced activity of PPARγ level when compared with the basal. Insulin (100 nM) was used as the positive control [53]. Increased expression of PPARγ induces adipocyte differentiation in 3T3-L1 cells whereas the suppression of PPARγ expression blocks the lipid formation [12]. In this study, analysis of the gene expression demonstrated that the 3T3-L1 cells treated with α-mangostin significantly downregulated the PPARγ  expression. Therefore, we can deduce that the reduction in PPARγmay be the key step in the inhibition of adipocyte differentiation [22] in 3T3-L1 and that the targeting of PPARγ could be the main mechanism for blocking of adipocyte differentiation by the α-mangostin.

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