Electroacupuncture modulates myocardial insulin signaling and inflammatory markers in a rat model of type 2 diabetes

作者
Xiaoxiao Liu,Haihua Zhang,Jian Sun,Xiao-zhuan Chen,Yang-yang Ye,Jinxing Quan,Lu Zhang,Linlin Nie,Min Li,Zhixing Li
出处
期刊:Acupuncture in Medicine [SAGE Publishing]
卷期号:44 (1): 36-48
标识
DOI:10.1177/09645284251399239
摘要

Objective: To evaluate the effects of electroacupuncture (EA) on myocardial insulin resistance (IR) in Zucker diabetic fatty (ZDF) rats, an established model for type 2 diabetes mellitus (T2DM). Methods: Twenty-four ZDF-Lepr fa/fa rats were randomized to: (1) ZDF group (n = 8); (2) ZDF + PIO (pioglitazone) group (n = 8); and (3) ZDF + EA group (n = 8). An additional control group of eight healthy ZDF +/fa rats was included (Lean group). We examined protein and mRNA expression levels of critical insulin signaling pathway intermediates including insulin receptor substrate (IRS)-1, phosphoinositide 3-kinase (PI3K), protein kinase B (Akt), adenosine monophosphate (AMP)-activated protein kinase (AMPK), ribosomal protein S6 kinase (p70S6K), glycogen synthase kinase 3β (GSK3β) and glucose transporter type 4 (GLUT4), as well as serum levels of interleukin (IL)-6, tumor necrosis factor (TNF)-α and C-reactive protein. Echocardiography and cardiac histology were performed. Results: Significant improvements in glucose metabolism, reflected in reduced fasting insulin levels and fasting blood glucose levels, were demonstrated after EA and PIO treatment. EA treatment also led to a notable decrease in inflammatory cytokine levels. In addition, there were marked improvements in myocardial structural integrity, as evidenced by histological analyses. Moreover, increased GLUT4 expression in myocardial tissue suggested improved insulin signaling, further supported by reductions in markers of myocardial injury such as serum troponin T type 2 (TNNT2) and B-type natriuretic peptide (BNP). Conclusion: EA ameliorated myocardial IR in a rat model of T2DM and positively impacted TNNT2 and BNP levels, as well as phosphorylation status and mRNA expression of several genes involved in the insulin signaling pathway. Our findings underscore the potential of EA to modulate multiple therapeutic targets in the treatment of myocardial IR. If these effects can be replicated clinically, EA may represent a promising non-pharmacological option for the management of cardiometabolic risks associated with diabetes.
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