Evidence for acupoint catgut embedding treatment and TRPV1 gene deletion increasing weight control in murine model

Abstract

Obesity is a global health problem affecting the general population. Acupoint catgut embedding (ACE) is an alternative treatment that involves the implantation of absorbable catgut suture at acupoints. The transient receptor vanilloid member 1 (TRPV1) is a calcium ion channel that responds to several chemical ligands and is identified in numerous locations throughout the body. The aim of the present study was to examine the effect of ACE treatment on obesity and its associated complications through various neural mechanisms in a murine model. A C57/BL6 wild type (WT) and TRPV1-/- (KO) mouse model was utilized to exclude any psychological factors associated with obesity. The WT-HFD-ACE and WT-HFD-SHAM groups received weekly ACE or placebo treatments at the bilateral ST36 acupoint. The mice were fed with a normal mice chow diet (ND) or a high-fat food diet (HFD; 45 kcal%), and their body weights were recorded once a week. After 8 weeks, the subjects were sacrificed and changes in the levels of a number of biomarkers were investigated using ELISA, immunoblotting and immunofluorescence. The results indicated a significant decrease in body weight variation for the WT-HFD-ACE group compared with the WT-HFD and WT-HFD. SHAM groups, using the WT-ND group as the body weight baseline. By contrast, KO mice fed with ND or HFD demonstrated notable body weight maintenance throughout the experimental period. Similar patterns were observed in adipose tissue mass, glucose, leptin and insulin plasma levels, and protein molecule density of TRPV1 and its associated molecules in the hypothalamus and nucleus tractus solitarii. In contrast, in the prefrontal cortex, significant decreases in the concentrations of MAPK pathway proteins in the WT-HFD and WT-HFD. SHAM groups were observed. The levels of these proteins were significantly increased in the WT-HFD-ACE and KO-HFD groups. These results suggested that TRPV1 and its associated pathways may be involved in body weight maintenance, and may be controlled through ACE treatment or genetic manipulation.