Antidiabetic Effects of Pterosin A, a Small-Molecular-Weight Natural Product, on Diabetic Mouse Models

Author:

Hsu Feng-Lin1,Huang Chun-Fa2,Chen Ya-Wen34,Yen Yuan-Peng5,Wu Cheng-Tien5,Uang Biing-Jiun6,Yang Rong-Sen7,Liu Shing-Hwa58

Affiliation:

1. Graduate Institute of Pharmacognosy, Taipei Medical University, Taipei, Taiwan

2. Graduate Institute of Chinese Medical Science, School of Chinese Medicine, China Medical University, Taichung, Taiwan

3. Department of Physiology, China Medical University, Taichung, Taiwan

4. Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan

5. Institute of Toxicology, College of Medicine, National Taiwan University, Taipei, Taiwan

6. Department of Chemistry, College of Science, National Tsing Hua University, Hsinchu, Taiwan

7. Department of Orthopaedics, College of Medicine, National Taiwan University, Taipei, Taiwan

8. Department of Urology, College of Medicine, National Taiwan University Hospital, Taipei, Taiwan

Abstract

The therapeutic effect of pterosin A, a small-molecular-weight natural product, on diabetes was investigated. Pterosin A, administered orally for 4 weeks, effectively improved hyperglycemia and glucose intolerance in streptozotocin, high-fat diet–fed, and db/db diabetic mice. There were no adverse effects in normal or diabetic mice treated with pterosin A for 4 weeks. Pterosin A significantly reversed the increased serum insulin and insulin resistance (IR) in dexamethasone-IR mice and in db/db mice. Pterosin A significantly reversed the reduced muscle GLUT-4 translocation and the increased liver phosphoenolpyruvate carboxyl kinase (PEPCK) expression in diabetic mice. Pterosin A also significantly reversed the decreased phosphorylations of AMP-activated protein kinase (AMPK) and Akt in muscles of diabetic mice. The decreased AMPK phosphorylation and increased p38 phosphorylation in livers of db/db mice were effectively reversed by pterosin A. Pterosin A enhanced glucose uptake and AMPK phosphorylation in cultured human muscle cells. In cultured liver cells, pterosin A inhibited inducer-enhanced PEPCK expression, triggered the phosphorylations of AMPK, acetyl CoA carboxylase, and glycogen synthase kinase-3, decreased glycogen synthase phosphorylation, and increased the intracellular glycogen level. These findings indicate that pterosin A may be a potential therapeutic option for diabetes.

Publisher

American Diabetes Association

Subject

Endocrinology, Diabetes and Metabolism,Internal Medicine

Reference50 articles.

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