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

被引:23
作者
Krisanapun, Chutwadee [1 ,2 ]
Lee, Seong-Ho [1 ]
Peungvicha, Penchom [2 ]
Temsiririrkkul, Rungravi [3 ]
Baek, Seung Joon [1 ]
机构
[1] Univ Tennessee, Coll Vet Med, Dept Pathobiol, Knoxville, TN 37996 USA
[2] Mahidol Univ, Fac Pharm, Dept Physiol, Bangkok 10700, Thailand
[3] Mahidol Univ, Fac Pharm, Dept Pharmaceut Bot, Bangkok 10700, Thailand
基金
美国国家卫生研究院;
关键词
HYPOGLYCEMIC ACTIVITY; INSULIN-RESISTANCE; SIGNALING PATHWAY; GLUCOSE-UPTAKE; EXTRACT; ADIPONECTIN; MECHANISMS; EXPRESSION; ALLOXAN; DISEASE;
D O I
10.1093/ecam/neq004
中图分类号
R [医药、卫生];
学科分类号
10 ;
摘要
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 PPAR. 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-3 beta 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 PPAR gamma agonist activity, and increasing glucose utilization via GLUT1.
引用
收藏
页码:1 / 9
页数:9
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