Gallic Acid Alleviates Hypertriglyceridemia and Fat Accumulation via Modulating Glycolysis and Lipolysis Pathways in Perirenal Adipose Tissues of Rats Fed a High-Fructose Diet.

Da-Wei Huang,James Wu,Szu-Chuan Shen,Heng-Jui Yang,Wen-Chang Chang

doi:10.3390/ijms19010254

Abstract

This study investigated the ameliorative effect of gallic acid (GA) on hypertriglyceridemia and fat accumulation in perirenal adipose tissues of high-fructose diet (HFD)-induced diabetic rats. The previous results showed that orally administered GA (30 mg/kg body weight) for four weeks significantly reduced the levels of plasma glucose and triglyceride (TG) in HFD rats. GA also markedly decreased the perirenal adipose tissues weight of HFD rats in present study (p < 0.05). Western blot assay indicated that GA restored expression of insulin signaling-related proteins, such as insulin receptor (IR), protein kinase C-zeta (PKC-ζ), and glucose transporter-4 (GLUT4) in the perirenal adipose tissues of HFD rats. Moreover, GA enhanced expression of glycolysis-related proteins, such as phosphofructokinase (PFK) and pyruvate kinase (PK), and increased the expression of lipolysis-related proteins, such as adipose triglyceride lipase (ATGL), which is involved in lipolysis in the perirenal adipose tissues of HFD rats. This study revealed that GA may alleviate hypertriglyceridemia and fat accumulation through enhancing glycolysis and lipolysis pathways in perirenal adipose tissues of HFD rats. These findings also suggest the potential of GA in preventing the progression of diabetes mellitus (DM) complications.

Highlights

Diabetes mellitus (DM) is one of the fastest growing chronic diseases and is caused by a deficiency in insulin secretion or by ineffectiveness in insulin action [1]
The aim of the present study is to investigate the effect of gallic acid (GA) on hypertriglyceridemia and fat accumulation in perirenal adipose tissues of High-fructose diet (HFD)-induced diabetic rats
The results indicated that HFD increased perirenal and epidydimal adipose weight by 71.6% and 84.5% in comparison to the normal group, respectively

Summary

Introduction

Diabetes mellitus (DM) is one of the fastest growing chronic diseases and is caused by a deficiency in insulin secretion or by ineffectiveness in insulin action [1]. More than 95% of diabetic patients have type 2 DM (T2DM), causing hyperglycemia via an ineffectiveness of insulin action or an inability to mount a normal response to insulin in peripheral cells, resulting in the symptoms of insulin resistance [3,4]. Long-term fructose intake may enhance oxidative stress, impair the antioxidant system, and increase lipid peroxidation [6,7]. It can be associated with the pathogenesis of metabolic syndrome, including insulin resistance, abdominal obesity, dyslipidemia, intraabdominal fat accumulation, fatty liver, inflammation, and endothelial dysfunction, resulting in T2DM [5]. High-fructose diet (HFD)-induced diabetic rats are widely used as an in vivo model to investigate the mechanism of therapy for T2DM-associated insulin resistance [8]

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Results

Conclusion