Xu Wanling, Li Junfeng, Ji Chang, Fang Danwei, Yao Lulu, Xu Nenggui, Yi Wei
South China Research Center for Acupuncture and Moxibustion, Medical College of Acu-Moxi and Rehabilitation, Guangzhou University of Chinese Medicine, Guangzhou, China.
The First Affiliated Hospital, Jinan University, Guangzhou, China.
Front Neurosci. 2023 Mar 21;17:1145079. doi: 10.3389/fnins.2023.1145079. eCollection 2023.
Insulin resistance (IR) is one of the common pathological manifestations of metabolic-related diseases, and the prevalence of relevant diseases is high. Acupuncture is beneficial to IR patients, but the central mechanism underlying this treatment remains unclear. This study provides mechanistic insights into how electroacupuncture (EA) improves IR through the response of Pro-opiomelanocortin (POMC) neurons to adiponectin (Adipo).
Glucose tolerance tests (GTT), Insulin tolerance tests (ITT) and fasting blood glucose (FBG) were detected by glucometer. Serum insulin, Adipo and skeletal muscle adiponectin receptor 1 (AdipoR1) protein levels were examined by ELISA. Homeostasis model assessment estimated insulin resistance (HOMA-IR) was calculated using the following formula: HOMA-IR = fasting insulin (FINS) (mU/L) × FBG (mmol/L)/22.5. The expression levels of AdipoR1 and Adipo mRNA in skeletal muscle were detected by real-time PCR quantification. The co-marking of c-Fos/AdipoR1 and POMC neurons were investigated using immunofluorescence. Spontaneous excitatory postsynaptic currents (sEPSCs) of POMC neurons and the response of POMC neurons to Adipo were detected via electrophysiology.
EA significantly ameliorated HFD-induced impairment of GTT, ITT, FBG, and HOMA-IR which was correlated with recovery of the expression level of AdipoR1 and Adipo in skeletal muscle. The improved response of POMC neurons to Adipo in the hypothalamus may be a key factor in correcting abnormal glucose tolerance and improving IR.
This study demonstrates that EA can ameliorate HFD-induced impaired glucose tolerance through improved response of POMC neurons to Adipo in the hypothalamus, providing insight into the central mechanism of improving IR through EA.
胰岛素抵抗（IR）是代谢相关疾病的常见病理表现之一，相关疾病的患病率较高。针刺对IR患者有益，但其治疗的核心机制尚不清楚。本研究为电针（EA）如何通过促肾上腺皮质激素原（POMC）神经元对脂联素（Adipo）的反应改善IR提供了机制性见解。
用血糖仪检测葡萄糖耐量试验（GTT）、胰岛素耐量试验（ITT）和空腹血糖（FBG）。用酶联免疫吸附测定法检测血清胰岛素、Adipo和骨骼肌脂联素受体1（AdipoR1）蛋白水平。采用以下公式计算稳态模型评估胰岛素抵抗（HOMA-IR）：HOMA-IR=空腹胰岛素（FINS）（mU/L）×FBG（mmol/L）/22.5。通过实时PCR定量检测骨骼肌中AdipoR1和Adipo mRNA的表达水平。采用免疫荧光法研究c-Fos/AdipoR1与POMC神经元的共标记。通过电生理学检测POMC神经元的自发性兴奋性突触后电流（sEPSCs）以及POMC神经元对Adipo的反应。
EA显著改善了高脂饮食（HFD）诱导的GTT、ITT、FBG和HOMA-IR损伤，这与骨骼肌中AdipoR1和Adipo表达水平的恢复相关。下丘脑POMC神经元对Adipo反应的改善可能是纠正异常糖耐量和改善IR的关键因素。
本研究表明，EA可通过改善下丘脑POMC神经元对Adipo的反应来改善HFD诱导的糖耐量受损，为通过EA改善IR的中枢机制提供了见解。
