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Antidiabetic Activities of Abutilon indicum (L.) Sweet Are Mediated by Enhancement of Adipocyte Differentiation and Activation of the GLUT1 Promoter.

Krisanapun C, Lee SH, Peungvicha P, Temsiririrkkul R, Baek SJ - Evid Based Complement Alternat Med (2011)

Bottom Line: To measure glucose uptake enhanced by insulin-like activity, we used rat diaphragm incubated with various concentrations of the crude extract and found that the extract enhances glucose consumption in the incubated solution.Our data also indicate that the crude extract and the fractions (water and butanol) did not affect the activity of kinases involved in Akt and GSK-3β pathways; however, the reporter assay showed that the crude extract could activate glucose transporter 1 (GLUT1) promoter activity.These results suggest that the extract from A. indicum L. may be beneficial for reducing insulin resistance through its potency in regulating adipocyte differentiation through PPARγ agonist activity, and increasing glucose utilization via GLUT1.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathobiology, College of Veterinary Medicine, University of Tennessee, 2407 River Drive, Knoxville, TN 37996, USA.

ABSTRACT
Abutilon indicum (L.) Sweet is an Asian phytomedicine traditionally used to treat several disorders, including diabetes mellitus. However, molecular mechanisms supporting the antidiabetic effect of A. indicum L. remain unknown. The aim of this study was to evaluate whether extract of A. indicum L. improves insulin sensitivity. First, we observed the antidiabetic activity of aqueous extract of the entire plant (leaves, twigs and roots) of A. indicum L. on postprandial plasma glucose in diabetic rats. The subsequent experiments revealed that butanol fractions of the extract bind to PPARγ and activate 3T3-L1 differentiation. To measure glucose uptake enhanced by insulin-like activity, we used rat diaphragm incubated with various concentrations of the crude extract and found that the extract enhances glucose consumption in the incubated solution. Our data also indicate that the crude extract and the fractions (water and butanol) did not affect the activity of kinases involved in Akt and GSK-3β pathways; however, the reporter assay showed that the crude extract could activate glucose transporter 1 (GLUT1) promoter activity. These results suggest that the extract from A. indicum L. may be beneficial for reducing insulin resistance through its potency in regulating adipocyte differentiation through PPARγ agonist activity, and increasing glucose utilization via GLUT1.

No MeSH data available.


Related in: MedlinePlus

The effect of butanol fraction of A. indicum to induce mRNA expression of the PPARγ target gene. 3T3-L1 preadipocyte cells were differentiated. Twenty-four hours before and during differentiation, cells were treated with vehicle control (DMSO) or 100 μg ml−1 of butanol fraction. mRNA expression of PPARγ, LPL, aP2, adiponectin and glyceraldehyde 3-phosphate dehydrogenase (GAPDH) were measured at Days 0, 2, 4, 6 and 8 of differentiation.
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fig4: The effect of butanol fraction of A. indicum to induce mRNA expression of the PPARγ target gene. 3T3-L1 preadipocyte cells were differentiated. Twenty-four hours before and during differentiation, cells were treated with vehicle control (DMSO) or 100 μg ml−1 of butanol fraction. mRNA expression of PPARγ, LPL, aP2, adiponectin and glyceraldehyde 3-phosphate dehydrogenase (GAPDH) were measured at Days 0, 2, 4, 6 and 8 of differentiation.

Mentions: Since butanol fraction binds to PPARγ and transactivates PPARγ activity, gene expression profiles were observed to elucidate whether the butanol fraction actually induces adipocyte differentiation through PPARγ activation. Twenty-four hours before and during differentiation, butanol fraction at 100 μg ml−1 was added to the medium for observation of its effects on gene expression during 3T3-L1 adipocyte differentiation. Dimethyl sulfoxide (DMSO) was used as vehicle control. As shown in Figure 4, cells treated with the butanol fraction increased the expression of PPARγ, aP2, and adiponectin at day 8, consistent with the previous data indicating that butanol fraction enhances PPARγ activity (Figure 3(b)). However, there was no change in mRNA level of lipoprotein lipase (LPL) throughout the differentiation.


Antidiabetic Activities of Abutilon indicum (L.) Sweet Are Mediated by Enhancement of Adipocyte Differentiation and Activation of the GLUT1 Promoter.

Krisanapun C, Lee SH, Peungvicha P, Temsiririrkkul R, Baek SJ - Evid Based Complement Alternat Med (2011)

The effect of butanol fraction of A. indicum to induce mRNA expression of the PPARγ target gene. 3T3-L1 preadipocyte cells were differentiated. Twenty-four hours before and during differentiation, cells were treated with vehicle control (DMSO) or 100 μg ml−1 of butanol fraction. mRNA expression of PPARγ, LPL, aP2, adiponectin and glyceraldehyde 3-phosphate dehydrogenase (GAPDH) were measured at Days 0, 2, 4, 6 and 8 of differentiation.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3094712&req=5

fig4: The effect of butanol fraction of A. indicum to induce mRNA expression of the PPARγ target gene. 3T3-L1 preadipocyte cells were differentiated. Twenty-four hours before and during differentiation, cells were treated with vehicle control (DMSO) or 100 μg ml−1 of butanol fraction. mRNA expression of PPARγ, LPL, aP2, adiponectin and glyceraldehyde 3-phosphate dehydrogenase (GAPDH) were measured at Days 0, 2, 4, 6 and 8 of differentiation.
Mentions: Since butanol fraction binds to PPARγ and transactivates PPARγ activity, gene expression profiles were observed to elucidate whether the butanol fraction actually induces adipocyte differentiation through PPARγ activation. Twenty-four hours before and during differentiation, butanol fraction at 100 μg ml−1 was added to the medium for observation of its effects on gene expression during 3T3-L1 adipocyte differentiation. Dimethyl sulfoxide (DMSO) was used as vehicle control. As shown in Figure 4, cells treated with the butanol fraction increased the expression of PPARγ, aP2, and adiponectin at day 8, consistent with the previous data indicating that butanol fraction enhances PPARγ activity (Figure 3(b)). However, there was no change in mRNA level of lipoprotein lipase (LPL) throughout the differentiation.

Bottom Line: To measure glucose uptake enhanced by insulin-like activity, we used rat diaphragm incubated with various concentrations of the crude extract and found that the extract enhances glucose consumption in the incubated solution.Our data also indicate that the crude extract and the fractions (water and butanol) did not affect the activity of kinases involved in Akt and GSK-3β pathways; however, the reporter assay showed that the crude extract could activate glucose transporter 1 (GLUT1) promoter activity.These results suggest that the extract from A. indicum L. may be beneficial for reducing insulin resistance through its potency in regulating adipocyte differentiation through PPARγ agonist activity, and increasing glucose utilization via GLUT1.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathobiology, College of Veterinary Medicine, University of Tennessee, 2407 River Drive, Knoxville, TN 37996, USA.

ABSTRACT
Abutilon indicum (L.) Sweet is an Asian phytomedicine traditionally used to treat several disorders, including diabetes mellitus. However, molecular mechanisms supporting the antidiabetic effect of A. indicum L. remain unknown. The aim of this study was to evaluate whether extract of A. indicum L. improves insulin sensitivity. First, we observed the antidiabetic activity of aqueous extract of the entire plant (leaves, twigs and roots) of A. indicum L. on postprandial plasma glucose in diabetic rats. The subsequent experiments revealed that butanol fractions of the extract bind to PPARγ and activate 3T3-L1 differentiation. To measure glucose uptake enhanced by insulin-like activity, we used rat diaphragm incubated with various concentrations of the crude extract and found that the extract enhances glucose consumption in the incubated solution. Our data also indicate that the crude extract and the fractions (water and butanol) did not affect the activity of kinases involved in Akt and GSK-3β pathways; however, the reporter assay showed that the crude extract could activate glucose transporter 1 (GLUT1) promoter activity. These results suggest that the extract from A. indicum L. may be beneficial for reducing insulin resistance through its potency in regulating adipocyte differentiation through PPARγ agonist activity, and increasing glucose utilization via GLUT1.

No MeSH data available.


Related in: MedlinePlus