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Electroacupuncture attenuates hepatic lipid accumulation via AMP-activated protein kinase (AMPK) activation in obese rats
  1. Meirong Gong1,
  2. Chen Cao1,
  3. Fengli Chen1,
  4. Qian Li1,
  5. Xiaolin Bi2,
  6. Yinong Sun1,
  7. Zhen Zhan3
  1. 1Department of Acupuncture and Moxibustion, Nanjing University of Chinese Medicine, Nanjing, China
  2. 2Department of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, China
  3. 3Department of Basic Medical Sciences, Nanjing University of Chinese Medicine, Nanjing, China
  1. Correspondence to Professor Zhen Zhan, Department of Basic Medical Sciences, Nanjing University of Chinese Medicine, 138 Xianlin Avenue, Nanjing 210023, China; njzhenzhan{at}sina.com

Abstract

Background Electroacupuncture (EA) may offer an effective alternative approach for the treatment of obesity. EA mobilizes energy stores, but its effect on hepatic lipid metabolism is unknown, and the underlying mechanisms remain unclear.

Objective To examine the effect of EA on hepatic lipid accumulation in diet-induced obese (DIO) rats, and to explore potential underlying mechanisms.

Methods Male Sprague-Dawley rats were fed a normal diet (control group, n=10) or a high-fat diet (HFD) for 12 weeks to induce obesity. Those exhibiting diet-induced obesity were subdivided into two groups, one receiving EA (DIO+EA group, n=10) and one left untreated (DIO group, n=10) and observed for a further 4 weeks. Body, liver and fat pad weight were measured, and liver injury was assessed histologically as well as by measuring serum values of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Hepatic triglyceride (TG) and total cholesterol were quantified by enzymatic colorimetric methods. Expression of liver AMP-activated protein kinase (AMPK), acetyl-coenzyme A carboxylase (ACC), and carnitine palmitoyltransferase (CPT-1) was measured by Western blotting.

Results EA treatment led to a reduction in body, liver and fat pad weight in DIO rats. This was accompanied by decreases in hepatic TG and total cholesterol values, fatty droplet accumulation, and serum concentrations of ALT and AST. Furthermore, EA treatment restored phosphorylation levels of AMPK (Thr172) and ACC (Ser79) inhibited by HFD, and increased CPT-1 expression.

Conclusions EA reduces HFD-induced hepatic lipid accumulation, an effect that appears to be mediated through AMPK signalling pathways. Our results shed new light on the mechanisms by which EA may reduce obesity.

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