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This Article Full Text Full Text (PDF) All Versions of this Article: 296/6/E1275    most recent 00092.2009v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Yin, J. Articles by Ye, J. PubMed PubMed Citation Articles by Yin, J. Articles by Ye, J.

Shilianhua extract inhibits GSK-3β and promotes glucose metabolism

¹Pennington Biomedical Research Center, Louisiana State University System; and ²Medicinal Plant Research Laboratory, School of Renewable Natural Resources, Louisiana State University Agricultural Center, Baton Rouge, Louisiana

Submitted 11 February 2009 ; accepted in final form 31 March 2009

The extract of plant Shilianhua (SLH; Sinocrassula indica Berge) is a component in a commercial product for control of blood glucose. However, it remains to be investigated whether the SLH extract enhances insulin sensitivity in a model of type 2 diabetes. To address this question, the SLH crude extract was fractionated into four parts on the basis of polarity, and bioactivities of each part were tested in cells. One of the fractions, F100, exhibited a strong activity in the stimulation of glucose consumption in vitro. Glucose consumption was induced significantly by F100 in 3T3-L1 adipocytes, L6 myotubes, and H4IIE hepatocytes in the absence of insulin. F100 also increased insulin-stimulated glucose consumption in L6 myotubes and H4IIE hepatocytes. It increased insulin-independent glucose uptake in 3T3-L1 adipocytes and insulin-dependent glucose uptake in L6 cells. The glucose transporter-1 (GLUT1) protein was induced in 3T3-L1 cells, and the GLUT4 protein was induced in L6 cells by F100. Mechanism study indicated that F100 induced GSK-3β phosphorylation, which was comparable with that induced by insulin. Additionally, the transcriptional activity of NF-B was inhibited by F100. In RAW 264.7 macrophages, mRNA expression of NF-B target genes (TNF and MCP-1) was suppressed by F100. In KK.Cg-A^y/+ mice, F100 decreased fasting insulin and blood glucose and improved insulin tolerance significantly. We conclude that the F100 may be a bioactive component in the SLH plant. It promotes glucose metabolism in vitro and in vivo. Inhibition of GSK-3β and NF-B may be the potential mechanism.

glycogen synthase kinase-3β; tumor necrosis factor-; monocyte chemotactic protein-1; nuclear factor-B; KK-A^y mice; insulin resistance