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Identification and Functional Implications of Sodium/Myo-inositol Cotransporter 1 in Pancreatic Beta-cells and Type 2 Diabetes Mellitus.

Identification and Functional Implications of Sodium/Myo-inositol Cotransporter 1 in Pancreatic Beta-cells and Type 2 Diabetes Mellitus.
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Ting Li SY, Wai Cheng ST, Zhang D, Leung PS,


Ting Li SY, Wai Cheng ST, Zhang D, Leung PS, (click to view)

Ting Li SY, Wai Cheng ST, Zhang D, Leung PS,

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Diabetes 2017 02 15() pii db160880
Abstract

Myo-inositol (MI), the precursor of the second messenger phosphoinositide (PI), mediates multiple cellular events. Rat islets exhibit active transport of MI, though 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 SMIT impaired glucose-stimulated insulin secretion by INS-1E cells, probably via down-regulation of PI signaling. Additionally, we found that 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. Based on 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.

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