ABSTRACT
Objective: This study investigated the influence of electroacupuncture (EA) and its potential underlying mechanisms on adipose tissue in obese mice. Methods: Three-week-old male C56BL/6 mice were randomly divided to feed or not to feed high-fat diet (HFD), named HFD group and chow diet (CD) group, respectively. After 12 weeks, CD and HFD mice were randomly divided into two groups, respectively, to receive or not receive EA for 4 weeks. Body weight (BW) was monitored. Intraperitoneal glucose tolerance test and metabolic chamber recordings were performed. Blood samples and adipose tissue were collected for the analysis of leptin, triglyceride levels, and fat browning-related proteins. Results: EA significantly reduced food intake, BW, and white adipose tissue (WAT)/BW ratio; decreased the adipocyte size and serum concentrations of triglyceride (TG) and cholesterol; and increased oxygen consumption in HFD mice. Compared with the CD mice, the HFD mice had elevated fasting serum glucose level and impaired glucose tolerance; however, these parameters were decreased by EA treatment. Meanwhile, EA promoted the protein and mRNA expressions of UCP1, PRDM16, and PGC-1α in adipose tissue, and activated sympathetic nerves via p-TH, A2AR, and ß3AR in white adipose tissue. Conclusions: EA reduced food intake, BW, TG, and cholesterol, and improved glucose tolerance in HFD mice. This ameliorative effect of EA on obesity-related symptoms associated with its promoted adipose tissue plasticity via activating sympathetic nerves.
ABSTRACT
OBJECTIVE: To investigate the effects of electroacupuncture (EA) on the expression of adenosine receptor (AR) in the white adipose tissue (WAT) of diet-induced obese (DIO) mice, so as to reveal a peripheral mechanism of EA underlying improvement of body weight. METHODS: Forty three-week-old C 57 BL/6 male mice were divided into normal diet group (n=12) and high fat diet group (n=28) randomly, and fed by normal diet and high fat diet for 12 weeks, respectively. In the high fat diet group, mice with body weight over 20% heavier than that of the normal diet group were considered as obese mice. The normal diet mice and the obese mice were divided into normal group (CD, n=5) and normal plus EA group (CD+EA, n=7), or obese group (HFD, n=6) and obese plus EA group (HFD+EA, n=12). The CD+EA group and the HFD+EA group were treated with EA at "Zusanli"(ST 36) and "Neiting"(ST 44, 2 Hz/15 Hz, 0.6-1.0 mA) for 20 min, 6 times a week for 4 weeks. Body weight, ratio of WAT/body weight were calculated, qPCR and Western blot were applied to detect mRNA and protein levels of adenosine receptors in the epididymal adipose tissue (Epi-WAT), respectively. RESULTS: Compared with the normal diet group, high fat diet significantly increased body weight in C 57 BL/6 mice after feeding for 12 weeks (P<0.01); 18 out of 28 mice in the high fat diet group were classified as obesity. After treatment, the body weight and the ratio of Epi-WAT/body weight of the HFD group were increased than those in the CD group (P<0.05), the change of body weight in the HFD group was bigger than that in the CD group (P<0.01). Compared with the HFD group, the body weight and the ratio of Epi-WAT/body weight of the HFD+EA group were decreased after EA (P<0.05), the change of body weight was also significantly increased (P<0.01). No significant differences were found among the four groups in the expression level of A1R mRNA (P>0.05). The expression of A3R mRNA in the HFD group was lower than that in the CD group (P<0.01), while the expressions of A2A R and A2BR proteins were decreased in the HFD group than in the CD group (P<0.01). In comparison with the HFD group, the expression levels of A2AR and A2BR mRNAs and proteins were significantly up-regulated in the HFD+EA group, respectively (P<0.05, P<0.01). CONCLUSIONS: EA intervention is able to reduce the body weight of DIO mice, which Feb be associated with its effects in regulating the expression of A2AR and A2BR in WAT, suggesting a new mechanism of EA in accelerating peripheral WAT metabolism.
