Abstract
The traditional Chinese medicine has long been used in the treatment of diabetes, one major disease threatening the public health. It has been reported that artemether exerts antidiabetic effects on type 2 diabetes in db/db mice, however the underlying mechanisms remain unknown. In the present study, we show that artemether regulates expression of related enzymes participating in the glucose and lipid metabolism in the liver of db/db mice, which could at least partly explain the improved glucose and lipid metabolism in artemether-treated mice. Additionally, artemether also regulates expression of glycogen synthesis related enzymes in the skeletal muscle of db/db mice, supporting its promotive role in glycogen synthesis. Mechanistically, artemether activates AMPK pathway as well as PI3K/Akt pathway in the liver and skeletal muscle of db/db mice, suggesting that these two signaling pathways are both involved in the antidiabetic effects of artemether on type 2 diabetes in db/db mice. In conclusion, our study connects the antidiabetic effects of artemether to the regulation of metabolic enzymes and signaling pathways, and also provides molecular basis for the potential application of artemether in treating type 2 diabetes.
Highlights
Type 2 diabetes mellitus (T2DM) is a metabolic disease accounting for more than 90% of all diabetes cases [1]
The primary antibodies against glucokinase, phosphoenolpyruvate carboxykinase (PEPCK), carnitine palmitoyl transferase 1 (CPT1), and β-actin were purchased from Santa Cruz; The primary antibodies against PPARα, fatty acid synthase (FAS), and GSK-3β were purchased from Abcam; The primary antibodies against glucose transporter 4 (GLUT4) and glycogen synthase (GYS) were purchased from Novus Biologicals; The primary antibodies against pACC1, acetyl-CoA carboxylase 1 (ACC1), phosphorylated AMPK (p-AMPK), AMPK, p-PI3K, PI3K, p-AKT, and AKT were purchased from Cell Signaling
The present study was designed to explore how artemether improves the glucose and lipid metabolism in db/db mice, focusing on examining the potential regulatory role of artemether in the protein expression of enzymes associated with glucose and lipid metabolism and metabolic signaling pathways, including AMPK and PI3K/Akt, in mouse liver and skeletal muscle
Summary
Type 2 diabetes mellitus (T2DM) is a metabolic disease accounting for more than 90% of all diabetes cases [1]. The prevalence of T2DM, in the developing countries, has been rapidly rising over the past three decades, and its number is estimated to reach 395 million by 2030, which represents 7.7% of the total population aged 20–79 years in the world [2]. T2DM is characterized by increased blood glucose level, in which insulin resistance and insulin secretion failure are recognized as two main pathological changes that underlie its development and progression [3, 4]. Some Western medicine such as sulfonylurea, biguanides and thiazolidinediones have been widely employed to control T2DM symptoms, their efficacy is limited and some side effects emerge, including increased appetite and weight [5, 6].
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