Berberine chloride ameliorated PI3K/Akt-p/SIRT-1/PTEN signaling pathway in insulin resistance syndrome-induced rats

胰岛素抵抗 内分泌学 内科学 胰岛素受体 胰岛素 蛋白激酶B PTEN公司 白色脂肪组织 脂肪组织 过剩4 PI3K/AKT/mTOR通路 生物 化学 医学 信号转导 生物化学
作者
Marwa El‐Zeftawy,Doaa A. Ghareeb,Rasha Saad,Salma Awad,Nihal M. Elguindy,Mohammed Elsayed
标识
DOI:10.1101/459610
摘要

Abstract Insulin resistance is one of dangerous factors as it leads to numerous metabolic disorders such as non-insulin dependent diabetes mellitus. It affects most tissues mainly adipose tissue, liver and muscle. Nowadays, berberine has several medical applications against diseases. The current study was carried out to identify the effect of berberine chloride (BER-chloride) on phosphatidyl inositol-3-kinase/ phosphorylated protein kinase B/ sirtuin type 1/ phosphatase and tension homologue (PI3K/Akt-p/SIRT-1/PTEN) pathway during insulin resistance phenomena. Insulin resistance model was performed in experimental rats by using high fat diet. Plasma glucose, serum insulin, lipid profiles, hepatic oxidative stress markers were estimated. Serum transaminases activities and kidney function tests were determined. Further, hepatic PI3K, AKt-p, SIRT-1; PTEN levels were assayed. The concentration of adiponectin in serum, hepatic tissue and white adipose tissue was determined. Moreover, fold change in hepatic insulin, insulin receptor and retinol binding protein-4 (RBP4) at molecular level was performed. Histopathological study of white adipose tissue was also determined. The results showed increase the rats’ body weights, blood glucose, homeostatic model assessment, glycated hemoglobin, insulin and lipid profiles levels in group of rats fed on high fat diet for eight weeks and this elevation was decreased after administration of BER-chloride for two weeks. Further, BER-chloride administration exhibited improvement of oxidative stress parameters, PI3K, AKt-p, SIRT-1 and PTEN. This was associated with down-regulation of RBP4. According to these data we conclude that, BER-chloride mediated several insulin signaling pathways that could be of therapeutic significance to insulin resistance.
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