Abnormalities in carbohydrate metabolism and the insulin resistance status have been associated with hypertension. We have previously described alterations in the sodium-coupled sugar absorption in an experimental model of hypertension; in the present work, we studied the regulation of the sodium-independent, GLUT5-facilitated D-fructose intestinal transport in this pathology. Spontaneously hypertensive rats (SHR) and their normotensive, genetic control Wistar-Kyoto (WKY) rats, were used. Kinetic studies, carried out in ileal brush-border membrane vesicles (BBMVs), revealed a significant reduction (P < 0.05) in the maximal rate of transport (V max) for D-fructose in SHR, which, on the other hand, showed unaltered values for the Michaelis constant (K m) and the diffusion constant (K d). Immunoblotting analysis revealed the existence of lower (P < 0.05) levels of GLUT5 in apical membranes from SHR, this reduction being similar to that of V max. Similarly, Northern blot studies on the abundance of GLUT5 mRNA from ileal enterocytes showed a decrease (P < 0.05) in hypertensive rats, following the same pattern mentioned above. Therefore, the impaired D-fructose intestinal absorption is another feature of SHR, and this decrease in D-fructose uptake correlates with a reduction in the abundance of the apical GLUT5 transporter, which is controlled at a transcriptional level.
The Journal of Membrane Biology – Springer Journals
Published: Jan 1, 2004
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