Oral Vanadate Reduces Na+-Dependent Glucose Transport in Rat Small Intestine

Abstract

The effects of oral vanadate supplementation on intestinal morphometry and glucose transport were examined in STZ-induced diabetic and age-matched control male Sprague-Dawley rats. Animals received 0.1 mg/ml vanadium pentoxide in their drinking water over 14 days. Vanadate reduced intestinal glucose maximal transport capacity in both diabetic and control animals. In jejunum tissue, this decrease in glucose absorption was a direct consequence of downregulation of the glucose carrier and was not related to changes in mucosal morphometry. In the ileum tissue of control animals, the vanadate-induced decrease in glucose maximal transport capacity occurred in conjunction with an increase in carrier affinity and mucosal morphometric measurements. In the ileum tissue of diabetic animals, the vanadate-induced decrease in glucose maximal transport capacity occurred with a decrease in mucosal morphometric measurements. Na(+)-K(+)-adenosine triphosphatase activity was affected by vanadate only in diabetic animals. These results demonstrate that oral vanadate supplementation results in downregulation of the small intestinal sodium-dependent glucose carrier in both diabetic and nondiabetic rats. Furthermore, the vanadate effect may be occurring at the cellular level.

Oral vanadyl sulfate improves hepatic and peripheral insulin sensitivity in patients with non-insulin-dependent diabetes mellitus.

“…Furthermore, we are not aware of published data that indicate that the minimal decline in body weight we observed during treatment can explain the marked changes in glucose metabolism. Other postulated effects include a reduction in Na+ -dependent glucose transport in small intestine (50). Previous studies from our laboratory indicated that vanadate treatment in diabetic rats improved the basal insulin receptor tyrosine kinase activity with no change in insulin-stimulated activity (10).…”

Vanadate treatment rapidly improves glucose transport and activates 6-phosphofructo-1-kinase in diabetic rat intestine

“…It is well documented that vanadate can prevent the changes produced in the small intestine by the induction of experimental diabetes [8] and this effect has generally been considered a secondary consequence of the reduction in hyperglycaemia induced by vanadate [9]. However, the concentration of vanadate used in this study (0.5 mg/ml) stabilized blood glucose levels at a slightly hyperglycaemic level, similar to results obtained by Sekar et al [21], while PFK 1 activity was normalized along the entire small intestine, and glucose transport was normalized in the jejunum.…”

“…Diabetic animals are hyperphagic and vanadate supplementation has previously been shown to reduce food intake [8]. To determine if a reduction in food intake may have contributed to the down-regulation of glucose transport, BBMV were prepared from animals which had been fasted for 12 h. As seen in Table 1, fasting had no effect on intestinal Na-dependent glucose transport.…”

“…Oral vanadate has also been shown to reduce Na-dependent glucose transport in the small intestine in normal rats and prevent the increase in transport from occurring in STZ-diabetic rats [8]. While there is evidence to suggest that oral vanadate is effective in restoring Na-dependent glucose transport to normal levels in the STZ-diabetic rat model [9], there have been no studies done to examine the effects of oral vanadate on intestinal PFK 1 activity and no studies to determine whether the jejunum and ileum response to vanadate is similar.…”

Sodium tungstate decreases sucrase and Na+/d-glucose cotransporter in the jejunum of diabetic rats

“…Tungstate did not affect this transporter in control rats, but there was a marked reduction in the activity and abundance of SGLT1 in the brushborder membrane of diabetic animals. The correlation between (22). In our study, the unchanged K m indicates that tungstate does not induce alterations in the structure or composition of the brush-border membrane.…”