Chinese Olive (Canarium album L.) Fruit Extract Attenuates Metabolic Dysfunction in Diabetic Rats.

Yu-Te Yeh,An-Na Chiang,Shu-Chen Hsieh

doi:10.3390/nu9101123

Abstract

Hyperglycemia and dysregulation of lipid metabolism play a crucial role in metabolic dysfunction. The aims of present study were to evaluate the ameliorative effect of the ethyl acetate fraction of Chinese olive fruit extract (CO-EtOAc) on high-fat diet (HFD) and streptozotocin (STZ)-induced diabetic rats. CO-EtOAc, rich in gallic acid and ellagic acid, could markedly decreased the body weight and epididymal adipose mass. In addition, CO-EtOAc increased serum HDL-C levels, hepatic GSH levels, and antioxidant enzyme activities; lowered blood glucose, serum levels of total cholesterol (TC), triglycerides (TG), bile acid, and tumor necrosis factor alpha (TNFα); and reduced TC and TG in liver. We further demonstrated that CO-EtOAc mildly suppressed hepatic levels of phosphorylated IRS-1, TNF-α, and IL-6, but enhanced Akt phosphorylation. The possible mechanisms of cholesterol metabolism were assessed by determining the expression of genes involved in cholesterol transportation, biosynthesis, and degradation. It was found that CO-EtOAc not only inhibited mRNA levels of SREBP-2, HMG-CoAR, SR-B1, and CYP7A1 but also increased the expression of genes, such as ABCA1 and LDLR that governed cholesterol efflux and cholesterol uptake. Moreover, the protein expressions of ABCA1 and LDLR were also significantly increased in the liver of rats supplemented with CO-EtOAc. We suggest that Chinese olive fruit may ameliorate metabolic dysfunction in diabetic rats under HFD challenge.

Highlights

Diabetes mellitus (DM) is one of the most common endocrine disorders and the third leading cause of death in developed countries [1]
We show that CO-EtOAc administration increased GSH levels and activities of superoxide dismutase (SOD), CAT, and glutathione peroxidase (GPx) in the livers of diabetic rats
This study demonstrated that treatment of CO-EtOAc decreased body weight gain and altered serum lipid and inflammatory profiles in high-fat diet (HFD)-fed combined with STZ-challenged diabetic rats

Summary

Introduction

Diabetes mellitus (DM) is one of the most common endocrine disorders and the third leading cause of death in developed countries [1]. Type 2 diabetes mellitus (T2DM) accounts for about. 90% to 95% of all diagnosed cases of diabetes [2]. Accumulating evidence indicates that obesity contributes to down-regulation of insulin secretion, defecting insulin action or both [3,4], which may disturb carbohydrate and lipid homeostasis [5]. T2DM is associated with the chronic inflammatory state [6]. Among traditional anti-diabetic drugs, metformin is the most used in clinical therapy, but the side effects such as lactic acidosis and permanent nerve damage, limit its application in certain populations [7]. Understanding the molecular mechanism underlying T2DM would definitely facilitate the development of treatment for T2DM [8]

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