Abstract
BackgroundPrevious studies had suggested that electroacupuncture (EA) can promote white adipose tissue (WAT) browning to counter obesity. But the mechanism was still not very clear.AimIn this study, we aim to study the effect of EA on promoting inguinal WAT (iWAT) browning and its possible mechanism.MethodThree-week-old rats were randomly divided into a normal diet (ND) group and a high-fat diet (HFD) group. After 10 weeks, the HFD rats were grouped into HFD + EA group and HFD control group. Rats in the EA group were electro-acupunctured for 4 weeks on Tianshu (ST25) acupoint under gas anesthesia with isoflurane, while the rats in HFD group were under gas anesthesia only. Body weight and cumulative food intake were monitored, and H&E staining was performed to assess adipocyte area. The effect of EA on WAT was assessed by qPCR, immunoblotting, immunoprecipitation and Co-immunoprecipitation. Mitochondria were isolated from IWAT to observe the expression of mitochondrial transcription factor A (TFAM).ResultsThe body weight, WAT/body weight ratio and cumulative food consumption obviously decreased (P < 0.05) in the EA group. The expressions of brown adipose tissue (BAT) markers were increased in the iWAT of EA rats. Nevertheless, the mRNA expressions of WAT genes were suppressed by 4-week EA treatment. Moreover, EA increased the protein expressions of SIRT-1, PPARγ, PGC-1α, UCP1 and PRDM16 which trigger the molecular conversion of iWAT browning. The decrease of PPARγ acetylation was also found in EA group, indicating EA could advance WAT-browning through SIRT-1 dependent PPARγ deacetylation pathway. Besides, we found that EA could activate AMPK to further regulate PGC-1α-TFAM-UCP1 pathway to induce mitochondrial biogenesis.ConclusionIn conclusion, EA can remodel WAT to BAT through inducing SIRT-1 dependent PPARγ deacetylation, and regulating PGC-1α-TFAM-UCP1 pathway to induce mitochondrial biogenesis. This may be one of the mechanisms by which EA affects weight loss.
Highlights
Obesity has become an epidemic concern and brought on global public health consequences, Over one third of U.S adults suffer from obesity [1], even 20–30% of entire populations have become obese in only 50 years [2], causing a series of severe comorbidities; for example, obesity was associated with a fivefold risk of type 2 diabetes regardless of genetic predisposition [3]
We aim to figure out whether EA can activate Sirtuin 1 (SIRT-1)-dependent PPARg deacetylation pathway and PGC-1aTFAM-UCP1 pathway to promote the browning of White adipose tissue (WAT) and mitochondria biogenesis, so as to combat obesity
After 10 weeks, obese rats were defined by a 20% increase in body weight compared to the normal diet group (ND) ones, and the rats in high-fat diet group (HFD) group were randomly reallocated into HFD group and HFD with electroacupuncture (HFD + EA) group
Summary
Obesity has become an epidemic concern and brought on global public health consequences, Over one third of U.S adults suffer from obesity [1], even 20–30% of entire populations have become obese in only 50 years [2], causing a series of severe comorbidities; for example, obesity was associated with a fivefold risk of type 2 diabetes regardless of genetic predisposition [3]. Ranging from drugs to calorie restriction, the existing antiobesity ways don’t yield the desired effect, among which white adipose tissue-browning intensified the interests in uncovering the underlying mechanisms due to its therapeutic potential for the remedy of metabolic diseases. It has been largely reported that WAT in rodents can undergo “browning” and acquire features of BAT following cold exposure [7], chronic endurance exercise [8, 9], and b3adrenergic stimulation [10]. This process had been mentioned as “browning” of WAT or WAT-browning.
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