Affiliation:
1. School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China
Abstract
Myo-inositol (MI), the precursor of the second messenger phosphoinositide (PI), mediates multiple cellular events. Rat islets exhibit active transport of MI, although the mechanism involved remains elusive. Here, we report, for the first time, the expression of sodium/myo-inositol cotransporter 1 (SMIT1) in rat islets and, specifically, β-cells. Genetic or pharmacological inhibition of SMIT1 impaired glucose-stimulated insulin secretion by INS-1E cells, probably via downregulation of PI signaling. In addition, SMIT1 expression in INS-1E cells and isolated islets was augmented by acute high-glucose exposure and reduced in chronic hyperglycemia conditions. In corroboration, chronic MI treatment improved the disease phenotypes of diabetic rats and islets. On the basis of our results, we postulate that the MI transporter SMIT1 is required to maintain a stable PI pool in β-cells in order that PI remains available despite its rapid turnover.
Funder
General Research Fund of
The Research Grants Council of the Hong Kong Special Administrative Region
Publisher
American Diabetes Association
Subject
Endocrinology, Diabetes and Metabolism,Internal Medicine
Cited by
10 articles.
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