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1 Gene Regulation, Pennington Biomedical Research Center/LSU, Baton Rouge, Louisiana, United States
2 Agricultural Center, LSU, Baton Rouge, Louisiana, United States
3 Agricultural Center, LSU, Baton Rouge, Louisiana, United States; Baton Rouge, Louisiana, United States
4 Baton Rouge, United States; Gene Regulation, Pennington Biomedical Research Center/LSU, Baton Rouge, Louisiana, United States
* To whom correspondence should be addressed. E-mail: yej{at}pbrc.edu.
Berberine, a botanical alkaloid used to control blood glucose in type 2 diabetes in China, has been reported to activate AMPK recently. However, it is not clear how AMPK is activated by berberine. In this study, activity and action mechanism of berberine were investigated in vivo and in vitro. In dietary obese rats, berberine increased insulin sensitivity after five week administration. Fasting insulin and HOMA-IR were decreased by 46% and 48% in the rats, respectively. In cell lines including 3T3-L1 adipocytes, L6 myotubes, C2C12 myotubes and H4IIE hepatocytes, berberine was found to increase glucose consumption, 2-deoxy-glucose uptake and to a less degree 3-O-methyl-glucose (3-OMG) uptake independently of insulin. The insulin-induced glucose uptake was enhanced by berberine in the absence of change in IRS-1 (S307/312), Akt, P70S6 and ERK phosphorylation. AMPK phosphorylation was increased by berberine at 0.5 h and the increase remained for at least 16 h. Aerobic and anaerobic respiration were determined to understand the mechanism of berberine action. The long-lasting phosphorylation of AMPK was associated with persistent elevation in AMP/ATP ratio and reduction in oxygen consumption. An increase in glycolysis was observed with a rise in lactic acid production. Berberine exhibited no cytotoxicity, and protected plasma membrane in L6 myotubes in the cell culture. These results suggest that berberine enhances glucose metabolism by stimulation of glycolysis, which is related to inhibition of glucose oxidation in mitochondria. Berberine-induced AMPK activation is likely a consequence of mitochondria inhibition that increases AMP/ATP ratio.
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