Abstract
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 (Vmax) for D-fructose in SHR, which, on the other hand, showed unaltered values for the Michaelis constant (Km) and the diffusion constant (Kd). 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 Vmax. 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.
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