Abstract

Type 2 diabetes mellitus (T2DM) is a chronic disease that has become a global public health problem. Studies on T2DM prevention and treatment mostly focus on discovering therapeutic drugs. Artemisinin and its derivatives were originally used as antimalarial treatments. In recent years, the roles of artemisinins in T2DM have attracted much attention. Artemisinin treatments not only attenuate insulin resistance and restore islet ß-cell function in T2DM but also have potential therapeutic effects on diabetic complications, including diabetic kidney disease, cognitive impairment, diabetic retinopathy, and diabetic cardiovascular disease. Many in vitro and in vivo experiments have confirmed the therapeutic utility of artemisinin and its derivatives on T2DM, but no article has systematically demonstrated the specific role artemisinin plays in the treatment of T2DM. This review summarizes the potential therapeutic effects and mechanism of artemisinin and its derivatives in T2DM and associated complications, providing a reference for subsequent related research.

Highlights

  • Diabetes mellitus is a group of metabolic disorders characterized by prolonged elevated blood glucose levels (Punthakee et al, 2018)

  • Artemisinic acid inhibits the expression and activity of gelatinase matrix metalloproteinase (MMP)-2, which is important to the development of adipose tissue (Croissandeau et al, 2002; Lee et al, 2012a). These results show that artemisinins inhibit adipocyte formation and differentiation by suppressing the master regulators CCAAT/enhancer-binding proteins (C/EBPs) and peroxisome proliferator-activated receptors (PPARs) γ and related molecules to improve insulin resistance (IR)

  • Artemisinins, except arteether, can pass through the bloodbrain barrier; we can infer from the experimental results of Albasher and Zeng that artemisinin may attenuate diabetic cognitive impairment (Zeng et al, 2017; Albasher et al, 2020)

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Summary

INTRODUCTION

Diabetes mellitus is a group of metabolic disorders characterized by prolonged elevated blood glucose levels (Punthakee et al, 2018). The researchers of this study concluded that relatively high concentrations of artemisinin and dihydroartemisinin may cause damage to pancreatic cells in obese patients but not in healthy individuals

A Controversial Mechanism: α-Cell to ß-Cell Transdifferentiation
Findings
DISCUSSION
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