Abstract
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.
Highlights
The thiazolidinedione (TZD) class of synthetic peroxisome proliferator-activated receptorγ (PPARγ) agonists is used widely in diabetes to increase insulin sensitivity
It was found that levels of fasted blood glucose (FBG), triglyceride, and total cholesterol in serum of the type 2 diabetes mellitus (T2DM) rats were significantly higher than those in the control group (Con) rats, accompanied by reduction in body weight
These indexes were similar to pathological state of type 2 diabetes, indicating the DM rats could be considered as type 2 diabetic rats [33, 34]
Summary
The thiazolidinedione (TZD) class of synthetic peroxisome proliferator-activated receptorγ (PPARγ) agonists is used widely in diabetes to increase insulin sensitivity. In addition to enhancing insulin activation, TZDs induce weight gain in humans and rodent models by enhancing adipogenesis and fluid retention and increasing food intake [3, 4]. Applied leptin in rodents induces a central signaling pathway that involves activation of signal transducer and activator of transcription 3 (STAT3) [29] The requirement of this pathway to prevent severe hyperphagia and obesity was recently demonstrated in mice lacking the STAT3-binding site of the leptin receptor [30] and in mice with reduced level of STAT3 protein selectively in the CNS [31]. The possible mechanism might be through increased leptin receptor and STAT3 and decreased PPARγ expressions in CNS, by which food intake of the rats was reduced and so that RSG-induced weight gain was inhibited
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