β-Lapachone Regulates Obesity through Modulating Thermogenesis in Brown Adipose Tissue and Adipocytes: Role of AMPK Signaling Pathway.

In this study, we explored the effect of β-Lapachone (βL), a compound obtained from the bark of the lapacho tree, against obesity. In vivo administration of βL into either high fat diet (HFD)-induced obese C57BL6 mice and genetically obese Lepr -∕- mice prevented body weight gain, which was associated with tissue weight loss of white adipose tissue (WAT). In addition, βL elevated thermogenic proteins including uncoupling protein 1 (UCP1) and mitochondrial count in BAT and human adipose tissue-derived mesenchymal stem cells (hAMSCs). βL also induced AMP-activated protein kinase (AMPK) phosphorylation, subsequent upregulation of acetyl-CoA carboxylase (ACC) and UCP1, and these effects were diminished by AMPK inhibitor compound C, suggesting that AMPK underlies the effects of βL. Mitogen-activated protein kinase pathways participated in the thermogenesis of βL, specifically p38, c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase 1/2 (ERK1/2) were activated by βL treatment in hAMSCs. Additionally, inhibitors of p38/JNK/ERK1/2 abrogated the activity of βL. Taken together, βL exerts anti-obese effects by inducing thermogenesis mediated by AMPK signaling pathway, suggesting that βL may have a potential therapeutic implication of obesity. Taken together, βL exerts anti-obese effects by not only inducing thermogenesis on brown adipocytes but also inducing the browning of white adipocytes. The anti-obese effect of βL is mediated by AMPK signaling pat...
Source: The American Journal of Chinese Medicine - Category: Complementary Medicine Authors: Tags: Am J Chin Med Source Type: research