The Role of Overexpressed Apolipoprotein AV in Insulin-Resistant Hepatocytes.

Wang Zhao,Xiaobo Liao,Shuiping Zhao,Yaqiong Liu

doi:10.1155/2020/3268505

Abstract

In this paper, we sought to explore the relationship between apolipoprotein AV (APOAV) overexpression and insulin resistance in hepatocytes. The insulin-resistant HepG2 cell model was constructed, and then, APOAV-overexpressed HepG2 cells (B-M) were induced by infecting with a recombinant adenovirus vector. Microarray data were developed from B-M samples compared with negative controls (A-con), and the microarray data were analyzed by bioinformatic methods. APOAV-overexpression induced 313 upregulated genes and 563 downregulated ones in B-M sample. The differentially expressed genes (DEGs) were significantly classified in fat digestion and absorption pathway. Protein-protein interaction network was constructed, and AGTR1 (angiotensin II receptor type 1) and P2RY2 (purinergic receptor P2Y, G-protein coupled 2) were found to be the significant nodes closely related with G-protein related signaling. Additionally, overexpression of APOAV could change the expression of Glut4 and release the insulin resistance of hepatic cells. Thus, APOAV overexpression may prevent the insulin resistance in liver cells by mediating the genes such as AGTR1 and P2RY2.

Highlights

Insulin resistance has become an increasingly common metabolic syndrome in people around the word. e main understanding of the mechanism for insulin resistance is the glycometabolism disorder in liver [1]
HepG2 cells, which are characterized by the common physiological function in glucose metabolism with normal hepatic cells [12], were used in this study. erefore, in the present study, we sought to explore the potential mechanism of relationship between apolipoprotein AV (APOAV) expression and insulin resistance in hepatocytes
We performed the microarray profiling of insulin-resistant HepG2 cells with APOAV overexpression to investigate the differential gene expression pattern induced by APOAV overexpression in comparison to the negative controls

Summary

Introduction

Insulin resistance has become an increasingly common metabolic syndrome in people around the word. e main understanding of the mechanism for insulin resistance is the glycometabolism disorder in liver [1]. E main understanding of the mechanism for insulin resistance is the glycometabolism disorder in liver [1]. Hyperglycemia is frequently associated with metabolic syndromes such as hypertension, coronary heart disease, and diabetes [3, 4]. Type 2 diabetes (T2D) is a common metabolic disorder that characterizes high blood sugar, insulin deficiency, and insulin resistance. APOAV is mainly expressed in liver and closely associated with high-density lipoprotein [8]. E decreased expression APOAV is involved in insulin resistance-related hypertriglyceridemia [6]. HepG2 cells, which are characterized by the common physiological function in glucose metabolism with normal hepatic cells [12], were used in this study. Erefore, in the present study, we sought to explore the potential mechanism of relationship between APOAV expression and insulin resistance in hepatocytes HepG2 cells, which are characterized by the common physiological function in glucose metabolism with normal hepatic cells [12], were used in this study. erefore, in the present study, we sought to explore the potential mechanism of relationship between APOAV expression and insulin resistance in hepatocytes

Materials and Methods

Verification Experiments

Results

Findings

Discussion