Electroacupuncture improves follicular development and metabolism and regulates the expression of adiponectin, AMPK and ACC in an obese rat model of polycystic ovary syndrome

内分泌学 内科学 多囊卵巢 脂联素 安普克 卵泡期 医学 高雄激素血症 AMP活化蛋白激酶 蛋白激酶A 生物 胰岛素抵抗 激酶 胰岛素 细胞生物学
作者
Jing Zhou,Ping Yin,Qingyi Zhao,Zhihai Hu,Yi Wang,Guizhi Ma,Xinyi Wu,Lu Lu,Yin Shi
出处
期刊:Acupuncture in Medicine [SAGE Publishing]
卷期号:41 (3): 151-162 被引量:6
标识
DOI:10.1177/09645284221107690
摘要

BACKGROUND: Polycystic ovary syndrome (PCOS) is a common endocrine disorder characterized by hyperandrogenism and follicular arrest. Electroacupuncture (EA) has been shown to be effective at improving hyperandrogenism and follicular arrest in PCOS; however, its mechanism of action remains to be deciphered. OBJECTIVE: In this study, we investigated whether EA improved follicular development in an obese rat model of PCOS and regulated the expression of adiponectin, AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC). METHODS: EA was administered at CV3, CV4 and ST40. Changes in body weight, paraovarian fat, estrus cycle, ovarian morphology, levels of related hormones, and glucose and lipid metabolism were evaluated. In addition, protein and mRNA expression of adiponectin, AMPK and ACC was measured. RESULTS: The body weight and paraovarian fat of rats in the EA group were reduced, while estrus cyclicity and ovarian morphology improved. Levels of free fatty acids, triglycerides, total cholesterol and low-density lipoprotein cholesterol were significantly reduced in the EA group, as well as blood glucose levels. Furthermore, levels of testosterone and luteinizing hormone were reduced in the EA group, while estradiol levels were increased. Protein and mRNA expression of adiponectin, AMPKα1 and liver kinase B1 (LKB1) was found to be increased in the EA group, while protein and mRNA expression of ACC were significantly reduced.Conclusion: Our findings suggest that EA improved follicular development and metabolism and regulated expression levels of adiponectin, AMPKα1, LKB1 and ACC in our obese rat model of PCOS.
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