Table of Contents Author Guidelines Submit a Manuscript
Evidence-Based Complementary and Alternative Medicine
Volume 2015, Article ID 142059, 12 pages
Research Article

A Cistanches Herba Fraction/β-Sitosterol Causes a Redox-Sensitive Induction of Mitochondrial Uncoupling and Activation of Adenosine Monophosphate-Dependent Protein Kinase/Peroxisome Proliferator-Activated Receptor γ Coactivator-1 in C2C12 Myotubes: A Possible Mechanism Underlying the Weight Reduction Effect

Division of Life Science, Hong Kong University of Science and Technology, Kowloon, Hong Kong

Received 29 August 2014; Accepted 14 January 2015

Academic Editor: Man Li

Copyright © 2015 Hoi Shan Wong et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Supplementary Material

Supplementary Table 1 and 2: The HCF1/BSS-induced AMPK activation in C2C12 myotubes was completely abrogated by co-incubation with either kCh or DMTU. A specific inhibitor of AMPK, CC, at a concentration of 10 µM, inhibited the HCF1/BSS-induced increase in PGC-1 nuclear translocation in C2C12 myotubes. The HCF1/BSS-induced nuclear translocation of PGC-1 was also prevented by co-incubation with either kCh or DMTU. The HCF1/BSS-induced elevations in UCP3 and COX levels were completely prevented by co-incubation of HCF1with kCh, DMTU or CC.

Supplementary Table 3: The possible role of mitochondrial uncoupling in HCF1-induced weight reduction was examined by the use of the chemical recoupler, kCh. HCF1 induced mitochondrial uncoupling in mouse skeletal muscle, as evidenced by the reduction in the mitochondrial RCR and the increase in mitochondrial UCP3 expression, in both ND- and HFD-fed mice. kCh per se significantly increased mitochondrial RCR in ND-fed mice. The HCF1-induced mitochondrial uncoupling in HFD-fed mice was completely inhibited by kCh co-treatment. HCF1 produced weight reduction in both ND- and HFD-fed mice. This effect was associated with the suppression of the HFD-induced increase in visceral fat index. In contrast to HCF1, kCh produced no detectable effect on weight gain in ND- and HFD-animals during the 8-week course of the experiment. The co-administration of kCh with HCF1 abolished the HCF1-induced suppressive effects on HFD-induced increase in body weight and visceral fat index in mice.

  1. Supplementary Material