Journal of Diabetes Mellitus

Volume 3, Issue 3 (August 2013)

ISSN Print: 2160-5831   ISSN Online: 2160-5858

Google-based Impact Factor: 0.48  Citations  

The effect of demethylasterriquinone B-1 on insulin secretion in rat pancreas

HTML  Download Download as PDF (Size: 836KB)  PP. 116-121  
DOI: 10.4236/jdm.2013.33017    2,916 Downloads   4,772 Views  Citations

ABSTRACT

A small nonpeptidyl compoud extracted from Pseudomassaria sp. was found to induce the activity of human insulin receptor tyrosine kinase in vitro. The compound was identified as demethylasterriquinone B-1 (DMAQ-B1). DMAQ- B1 also induced an increase in [Ca2+]i and insulin secretion in mice pancreatic beta-cells at low glucose (3 mM) concentration via insulin receptor substrate-1/phosphatidylinositol-3-kinase (PI3 kinase) pathway. By using rat pancreatic perfusion technique, we found that 10 μM DMAQ-B1 directly stimulated insulin secretion up to 240% in normal rat pancreas. In the dosage from 1 to 20 μM, DMAQ-B1 stimulated insulin secretion in a dose dependent manner. Furthermore, DMAQ-B1 enhanced glucose-induced insulin secretion by 17.6% (first stage) and 19.0% (second stage), respectively. The PI3 kinase inhibitors, LY 294002 (3.9 μM) or wortmannin (100 nM), inhibited DMAQ-B1-induced insulin secretion by 46.3% and 57.4%, respectively. LY 294002 or wortmannin also inhibited DMAQ-B1 with10 mMglucose-induced insulin secretion by 70.3% and 79.0%, respectively. All the results suggested that DMAQ-B1 directly stimulated insulin secretion and enhanced glucose-induced insulin secretion. The effect of DMAQ-B1 may mediate through the activation of PI3 kinase pathway to stimulate insulin secretion in normal rat pancreas.

Share and Cite:

Lai, M. , Lo, Y. and Yang, C. (2013) The effect of demethylasterriquinone B-1 on insulin secretion in rat pancreas. Journal of Diabetes Mellitus, 3, 116-121. doi: 10.4236/jdm.2013.33017.

Copyright © 2024 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.