Jing Xinyue, Ou Chen, Chen Hui, Wang Tianlin, Xu Bin, Lu Shengfeng, Zhu Bing-Mei
Key Laboratory of Acupuncture and Medicine Research of Ministry of Education, Nanjing University of Chinese Medicine, Nanjing 210023, China.
Key Laboratory of Acupuncture and Medicine Research of Ministry of Education, Nanjing University of Chinese Medicine, Nanjing 210023, China; Jiangxi University of Traditional Chinese Medicine, Nanchang 330004, China.
Evid Based Complement Alternat Med. 2016;2016:8098561. doi: 10.1155/2016/8098561. Epub 2016 Jan 20.
We investigate the effect of electroacupuncture (EA) on protecting the weight gain side effect of rosiglitazone (RSG) in type 2 diabetes mellitus (T2DM) rats and its possible mechanism in central nervous system (CNS). Our study showed that RSG (5 mg/kg) significantly increased the body weight and food intake of the T2DM rats. After six-week treatment with RSG combined with EA, body weight, food intake, and the ratio of IWAT to body weight decreased significantly, whereas the ratio of BAT to body weight increased markedly. HE staining indicated that the T2DM-RSG rats had increased size of adipocytes in their IWAT, but EA treatment reduced the size of adipocytes. EA effectively reduced the lipid contents without affecting the antidiabetic effect of RSG. Furthermore, we noticed that the expression of PPARγ gene in hypothalamus was reduced by EA, while the expressions of leptin receptor and signal transducer and activator of transcription 3 (STAT3) were increased. Our results suggest that EA is an effective approach for inhibiting weight gain in T2DM rats treated by RSG. The possible mechanism might be through increased levels of leptin receptor and STAT3 and decreased PPARγ expression, by which food intake of the rats was reduced and RSG-induced weight gain was inhibited.
我们研究了电针(EA)对2型糖尿病(T2DM)大鼠罗格列酮(RSG)体重增加副作用的保护作用及其在中枢神经系统(CNS)中的可能机制。我们的研究表明,RSG(5mg/kg)显著增加了T2DM大鼠的体重和食物摄入量。RSG联合EA治疗六周后,体重、食物摄入量以及附睾白色脂肪组织(IWAT)与体重的比值显著降低,而棕色脂肪组织(BAT)与体重的比值显著增加。苏木精-伊红(HE)染色表明,T2DM-RSG大鼠IWAT中脂肪细胞大小增加,但EA治疗减小了脂肪细胞大小。EA有效降低了脂质含量,同时不影响RSG的降糖作用。此外,我们注意到EA降低了下丘脑过氧化物酶体增殖物激活受体γ(PPARγ)基因的表达,同时增加了瘦素受体以及信号转导和转录激活因子3(STAT3)的表达。我们的结果表明,EA是抑制RSG治疗的T2DM大鼠体重增加的有效方法。其可能机制可能是通过增加瘦素受体和STAT3的水平以及降低PPARγ表达,从而减少大鼠的食物摄入量并抑制RSG诱导的体重增加。