Impact of erythropoietin and myoinositol versus metformin on insulin resistance in a rat model of polycystic ovary syndrome.

IF 2.5 4区医学 Q3 ENDOCRINOLOGY & METABOLISM

Archives of Physiology and Biochemistry Pub Date : 2024-02-01 Epub Date: 2021-07-23 DOI:10.1080/13813455.2021.1949023

Amany Abdelrahman, Aida Abdeen Mahmoud, Youstina Lamie Fanous, Nesreen Gamal Abd Elhaliem, Hassan Elalaf

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Abstract

This study aimed to evaluate the therapeutic role of erythropoietin (EPO) or myoinositol versus metformin (MET) in improving the reproductive functions and glucose tolerance in a rat model of polycystic ovary (PCOS). Oral letrozole (LTZ) was used for induction of PCOS in wester rats for 21 days, after that, MET, EPO and myoinositol were administered for the following 21 days. The LTZ-induced PCOS rats have lost their oestrous cyclicity and become fixed at the diestrus phase, developed insulin resistance, abnormal sex and gonadotrophin hormone serum levels, increased cystic follicles, decreased number of the growing follicles and very little or no corpora lutea on microscopic examination, which were reversed by the three drugs, MET, EPO and myoinositol. MET and myoinositol were mostly equally effective in improving the reproductive manifestations of the disease. However, EPO was most effective in decreasing the insulin level observed in this LTZ-induced model of PCOS.

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红细胞生成素和肌醇与二甲双胍对多囊卵巢综合征大鼠模型中胰岛素抵抗的影响

本研究旨在评估促红细胞生成素（EPO）或肌醇与二甲双胍（MET）在改善多囊卵巢（PCOS）大鼠模型的生殖功能和葡萄糖耐量方面的治疗作用。用口服来曲唑（LTZ）诱导大鼠多囊卵巢综合征 21 天，然后再给大鼠服用二甲双胍（MET）、EPO 和肌醇 21 天。LTZ诱导的多囊卵巢综合征大鼠失去了发情周期，固定在发情期，出现胰岛素抵抗，性激素和促性腺激素血清水平异常，囊性卵泡增多，生长卵泡数量减少，显微镜检查发现黄体极少或无黄体，MET、EPO和肌醇三种药物可逆转这些症状。MET 和肌醇在改善该病的生殖表现方面效果相当。然而，EPO在降低LTZ诱导的多囊卵巢综合症模型中观察到的胰岛素水平方面最为有效。

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来源期刊

Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY

CiteScore

6.90

自引率

3.30%

发文量

期刊介绍： Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.