The Aqueous Extract of Gynura divaricata (L.) DC. Improves Glucose and Lipid Metabolism and Ameliorates Type 2 Diabetes Mellitus.

Jinnan Li,Bo Zhang,Qunying Liu,Shengpan Hou,Jinlei Feng,Ying Zhao,Hong Wei,Ting Yang,Cheng Yang

doi:10.1155/2018/8686297

Abstract

Type 2 diabetes mellitus (T2DM) is a chronic disease characterized by hyperglycemia and dyslipidemia caused by impaired insulin secretion and resistance of the peripheral tissues. A major pathogenesis of T2DM is obesity-associated insulin resistance. Gynura divaricata (L.) DC. (GD) is a natural plant and has been reported to have numerous health-promoting effects on both animals and humans. In this study, we aimed to elucidate the regulatory mechanism of GD improving glucose and lipid metabolism in an obesity animal model induced by high-fat and high-sugar diet in combination with low dose of streptozocin and an insulin-resistant HepG2 cell model induced by dexamethasone. The study showed that the water extract of GD (GD extract A) could significantly reduce fasting serum glucose, reverse dyslipidemia and pancreatic damage, and regulate the body weight of mice. We also found that GD extract A had low toxicity in vivo and in vitro. Furthermore, GD extract A may increase glucose consumption in insulin-resistant HepG2 cells, markedly inhibit NF-κB activation, and decrease the impairment in signaling molecules of insulin pathway, such as IRS-1, AKT, and GLUT1. Overall, the results indicate that GD extract A is a promising candidate for the prevention and treatment of T2DM.

Highlights

Type 2 diabetes mellitus (T2DM), known as non-insulindependent diabetes mellitus, is a chronic metabolic disease and accounts for 90–95% of all diabetes patients [1]
Abnormal activation in the inflammation pathway often leads to elevated expression of a variety of inflammatory factors that switch on insulin resistance phenotype, which is essential for T2DM progression [7]
Tumor necrosis factor-α (TNF-α), IL-6, and PKC, as well as IK kinase, cause serine phosphorylation of downstream IR substrate family members IRS-1, inhibiting phosphatidylinositol 3kinase (PI3K) and serine/threonine kinase B (AKT), which leads to insulin resistance [12]

Summary

Introduction

Type 2 diabetes mellitus (T2DM), known as non-insulindependent diabetes mellitus, is a chronic metabolic disease and accounts for 90–95% of all diabetes patients [1]. Obesity is closely associated with an increased risk of developing insulin resistance and may be proven to be the biggest risk factor in causing T2DM [5]. Previous studies suggested that chronic inflammation may underlie the metabolic disorders of obesity-induced insulin resistance and T2DM [6, 7]. Abnormal activation in the inflammation pathway often leads to elevated expression of a variety of inflammatory factors that switch on insulin resistance phenotype, which is essential for T2DM progression [7]. TNF-α, IL-6, and PKC, as well as IK kinase, cause serine phosphorylation of downstream IR substrate family members IRS-1, inhibiting phosphatidylinositol 3kinase (PI3K) and serine/threonine kinase B (AKT), which leads to insulin resistance [12]. Inhibiting the NFκB and improving IRS/p-AKT signal pathway are a promising therapeutic strategy for effective treatment of T2DM

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Results