The short-circuit current of the ileum, but not the colon, is altered in the streptozotocin diabetic rat

Abstract

Ion transport in control and streptozotocin-diabetic rat colon and ileum was studied using the Ussing chamber technique. No differences were observed between control and diabetic colonic mucosal short-circuit current under either basal or carbachol (100 nmol/L – 1 µmol/L)-stimulated or prostaglandin E2 (100 nmol/L – 1 µmol/L)-stimulated conditions. Similarly to colonic tissues, no differences in the short circuit current in either carbachol-stimulated or prostaglandin E2-stimulated tissues were observed between control and diabetic ileal mucosa. The basal diabetic ileal short circuit current (99.58 ± 22.67 μA) was significantly greater than that of control ileal tissues (29.67 ± 4.45 μA). This difference was abolished by the sodium–glucose-cotransporter inhibitor, phloridzin (50 µmol/L) (118.00 ± 28.09 μA vs. 25.60 ± 4.59 μA) and was also prevented by the replacement of glucose with mannitol in the buffer bathing the apical side of the tissue (control: 17.05 ± 5.85 μA vs. 17.90 ± 3.10 μA). Acetazolamide (450 µmol/L; a carbonic anhydrase inhibitor), amiloride, and bumetanide (100 µmol/L each; Na+-channel blockers), piroxicam (50 µmol/L; a COX1 cyclooxygenase inhibitor), and ouabain (1 mmol/L; a K+ transport inhibitor) had no effect on the basal short circuit current of either control or diabetic ileal tissues. This indicated that the alteration in the basal short circuit current of diabetic ileal tissues was due to a change in cellular glucose transport, whereas the evoked changes in short circuit current were unaffected by the diabetic state.