Abstract
Myo‐inositol (MI) uptakes in cells is essentially performed by two Na+‐coupled transport systems; SMIT1, a basolateral system inducible through hypertonicity and SMIT2, an apical system responsible for MI uptake in the kidney and intestine, amongst other tissues. In diabetes, urinary MI excretion is increased by 1 order of magnitude through a non‐established mechanism. The purpose of this study is thus to investigate the influence of an acute diabetic condition (5‐day streptozotocintreatment) on the expression of both SMIT mRNA's in rat brain, liver, muscle, kidney and intestine through quantitative‐RT‐PCR (qRT‐PCR). Also, SMIT2 activity was determined by measuring MI transport in purified brush border membranes (BBMv) from kidney and intestine. SMIT1 transcripts are mainly found in the kidney where it doubles in diabetic rats. Other tissues show more modest mRNA levels and were not altered in diabetes. SMIT2 transcripts were found in all tested tissues in varying levels but were not modified in diabetes. MI uptakes performed on kidney and intestine BBMv confirmed the qRT‐PCR results showing no variations of transport in STZ rats due to SMIT2. We thus conclude that the increase in MI urinary excretion is not due to a reduction in the apical expression of MI cotransporter SMIT2.
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