BACKGROUND Electroacupuncture(EA)has been recognized for its beneficial effects on glucolipid metabolism,potentially through the regulation of sensory nerve coordination.The expandability of peripancreatic adipose tis...BACKGROUND Electroacupuncture(EA)has been recognized for its beneficial effects on glucolipid metabolism,potentially through the regulation of sensory nerve coordination.The expandability of peripancreatic adipose tissue(PAT)is implicated in the transition from obesity to type 2 diabetes mellitus(T2DM).However,the specific pancreatic responses to EA require further elucidation.AIM To investigate the influence of EA on pancreatic glucolipid reduction level in a high-fat diet(HFD)rat model.METHODS To delineate the precise pathway through which EA mediates interactions bet ween PAT and islets,we assessed the expression levels of NGF,TRPV1,insulin,as well as other proteins in the pancreas and PAT.This approach enabled us to identify the acupoints that are most conducive to optimizing glycolipid metabolism.RESULTS The ST25,LI11 and ST37 groups attenuated HFD-induced obesity and insulin resistance(IR)to distinct degrees,with ST25 group having the greatest effect.EA at ST25 was found to modify the local regulatory influence of PAT on the pancreatic intrinsic nervous system.Specifically,EA at ST25 obviously activated the TRPV1-CGRP-islet beta cell pathway,contributing to the relief of glucolipid metabolic stress.The beneficial effects were abrogated following the chemical silencing of TRPV1 sensory afferents,confirming their indispensable role in EA-mediated regulation of islet and PAT function.Furthermore,in TRPV1 knockout mice,a reduction in PAT inflammation was observed,along with the recovery of islet beta cell function.EA at LI11 and ST37 demonstrated anti-inflammatory properties and helped ameliorate IR.CONCLUSION The PAT ecological niche influenced the progression from obesity to T2DM through various immunometabolic pathways.EA at ST25 could regulate glucolipid metabolism via the TRPV1-CGRP-islet beta cell pathway.展开更多
基金Supported by National Natural Science Foundation of China,No.82305376,No.82374577,No.82305375,No.82074532,and No.82405567The Priority Academic Program Development of Jiangsu Higher Education Institutions(PAPD).
文摘BACKGROUND Electroacupuncture(EA)has been recognized for its beneficial effects on glucolipid metabolism,potentially through the regulation of sensory nerve coordination.The expandability of peripancreatic adipose tissue(PAT)is implicated in the transition from obesity to type 2 diabetes mellitus(T2DM).However,the specific pancreatic responses to EA require further elucidation.AIM To investigate the influence of EA on pancreatic glucolipid reduction level in a high-fat diet(HFD)rat model.METHODS To delineate the precise pathway through which EA mediates interactions bet ween PAT and islets,we assessed the expression levels of NGF,TRPV1,insulin,as well as other proteins in the pancreas and PAT.This approach enabled us to identify the acupoints that are most conducive to optimizing glycolipid metabolism.RESULTS The ST25,LI11 and ST37 groups attenuated HFD-induced obesity and insulin resistance(IR)to distinct degrees,with ST25 group having the greatest effect.EA at ST25 was found to modify the local regulatory influence of PAT on the pancreatic intrinsic nervous system.Specifically,EA at ST25 obviously activated the TRPV1-CGRP-islet beta cell pathway,contributing to the relief of glucolipid metabolic stress.The beneficial effects were abrogated following the chemical silencing of TRPV1 sensory afferents,confirming their indispensable role in EA-mediated regulation of islet and PAT function.Furthermore,in TRPV1 knockout mice,a reduction in PAT inflammation was observed,along with the recovery of islet beta cell function.EA at LI11 and ST37 demonstrated anti-inflammatory properties and helped ameliorate IR.CONCLUSION The PAT ecological niche influenced the progression from obesity to T2DM through various immunometabolic pathways.EA at ST25 could regulate glucolipid metabolism via the TRPV1-CGRP-islet beta cell pathway.
