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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

Stained fat droplets after differentiation programme (magnification 200x). (a) Insulin. (b) DMSO (negative control). (c) MDI-treated cells. ((d)–(f)) α-Mangostin, 10, 25, and 50 μM, respectively.
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fig2: Stained fat droplets after differentiation programme (magnification 200x). (a) Insulin. (b) DMSO (negative control). (c) MDI-treated cells. ((d)–(f)) α-Mangostin, 10, 25, and 50 μM, respectively.

Mentions: Eight days after treatment, preadipocytes differentiation was terminated and stained with Oil Red O. Fat droplets in these cells were visualised and photographed (Figure 2). Quantification of lipid accumulation by using UV spectrophotometer at 520 nm showed that cells treated with α-mangostin reduced intracellular fat accumulation dose-dependently up to 44.4% relative to MDI-treated control cells at the dose of 50 μM (Figure 3). Therefore, our results demonstrated that α-mangostin added to the adipocyte inducer (IBMX, dexamethasone, and insulin) showed antiadipogenic activity as evidenced by decreased triglyceride accumulation in 3T3-L1 cells at all of the tested concentrations. This unique mechanism of decreased lipid formation [19] by α-mangostin further prompted us to study the characteristic effect of α-mangostin on adipocyte differentiation by using the quantitative RT-PCR. Since most studies have shown that PPARγ is one of the target genes in the induction of adipocyte differentiation [11], owing to the same fact, the same gene was used to determine the mechanism for the inhibitory effect of α-mangostin on the 3T3-L1 cells.


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)

Stained fat droplets after differentiation programme (magnification 200x). (a) Insulin. (b) DMSO (negative control). (c) MDI-treated cells. ((d)–(f)) α-Mangostin, 10, 25, and 50 μM, respectively.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig2: Stained fat droplets after differentiation programme (magnification 200x). (a) Insulin. (b) DMSO (negative control). (c) MDI-treated cells. ((d)–(f)) α-Mangostin, 10, 25, and 50 μM, respectively.
Mentions: Eight days after treatment, preadipocytes differentiation was terminated and stained with Oil Red O. Fat droplets in these cells were visualised and photographed (Figure 2). Quantification of lipid accumulation by using UV spectrophotometer at 520 nm showed that cells treated with α-mangostin reduced intracellular fat accumulation dose-dependently up to 44.4% relative to MDI-treated control cells at the dose of 50 μM (Figure 3). Therefore, our results demonstrated that α-mangostin added to the adipocyte inducer (IBMX, dexamethasone, and insulin) showed antiadipogenic activity as evidenced by decreased triglyceride accumulation in 3T3-L1 cells at all of the tested concentrations. This unique mechanism of decreased lipid formation [19] by α-mangostin further prompted us to study the characteristic effect of α-mangostin on adipocyte differentiation by using the quantitative RT-PCR. Since most studies have shown that PPARγ is one of the target genes in the induction of adipocyte differentiation [11], owing to the same fact, the same gene was used to determine the mechanism for the inhibitory effect of α-mangostin on the 3T3-L1 cells.

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