Abstract
Acupuncture has thousands of years of history and perspective for the treatment of many health problems and disorders. Beneficial effects of acupuncture on obesity have been demonstrated at various levels in animals and clinical trials, with almost no adverse effect, even when combined with local electrical stimulation, i.e., electroacupuncture (EA), a way to potentiate the effects of acupuncture. However, there is still scattered evidence about the impact of EA on brain functions related to the control of eating behavior, and notably on the gut–brain axis mechanisms involved in these putative central modulations. During the past 10 years, we have described a convincing diet-induced obese minipig model, and successfully implemented brain imaging and neurocognitive approaches to challenge mechanistic hypotheses and innovative therapeutic strategies. In the present article, we propose to confront the current literature on the acupuncture and EA effects on the gut–brain axis and obesity with the latest developments in nutrition and neuroscience research using the minipig model. Our aims are to (a) elaborate functional hypotheses on the gut–brain mechanisms underlying EA effects on obesity, and especially on the role of the vagus nerve, and (b) present the rational for testing these hypotheses in the minipig model.
Highlights
Obesity involves a variety of pathogenesis affecting brain functions, gut hormones, the autonomic nervous system, low-grade inflammation and many other biological processes [1–3]
On the basis of the aforementioned state of the art, we propose implementing EA in the diet-induced obese minipig model to identify the best combination of acupoint stimulation to modulate brain areas involved in the different dimensions of food intake control
The prefrontal cortex and hippocampus were repeatedly found altered in minipig models of deleterious nutrition and obesity [11, 30, 40, 91], and we hypothesize that regulating their activity via EA at Baihui (GV20), in combination with EA-induced activation of the gut–brain vagal pathway, would contribute to regulate the behavioral and brain processes underlying food intake control, exactly as the more invasive vagus nerve stimulation did in the minipig model [41–43] (Fig. 2a)
Summary
Obesity involves a variety of pathogenesis affecting brain functions, gut hormones, the autonomic nervous system, low-grade inflammation and many other biological processes [1–3]. Previous research in the pig model showed that chronic abdominal vagal stimulation reduced food intake as a consequence of the activation of the brainstem and higher-order brain areas (prefrontal cortex, thalamus, insular cortex, superior colliculus, cingulate cortex) [41, 42] (Fig. 2a) In obese minipigs, this treatment was associated with reduced weight gain and preference for a sweet feed [43]. EA stimulation may generate physiological effects on the autonomic nervous system and especially the vagus nerve, which innervates many internal organs and further triggers brain response (Fig. 1a), with the consequence of regulating metabolic parameters, homeostasis, and eventually eating behavior (Fig. 1b). On the basis of the aforementioned state of the art, we propose implementing EA in the diet-induced obese minipig model to identify the best combination of acupoint stimulation to modulate brain areas involved in the different dimensions of food intake control (i.e., homeostasis, hedonism, and executive functions). Zheng et al [89] showed that EA at Baihui (GV20) normalized responses
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Eating and Weight Disorders - Studies on Anorexia, Bulimia and Obesity
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
