Insulin-Treatment of Diabetic Rats: Effects on Duodenal Calcium Absorption

Abstract

The hypothesis that depressed duodenal Ca absorption in the streptozotocin diabetic rat is the consequence of diabetes rather than nephrotoxicity of the diabetogenic agent causing abnormal renal vitamin D metabolism was tested. Streptozotocin diabetic rats were treated with insulin, their duodenal Ca transport response was compared with that of untreated diabetics and matched controls. Insulin treatment restored depressed Ca transport of diabetics to control levels in in vivo studies and significantly increased Ca transport in vitro. Previous studies showed that even in uncontrolled diabetes the mucosa retains the ability to respond to an end organ stimulus enhancing Ca transport: 1,25-dihydroxycholecalciferol corrects the defect, but vitamin D and 25-hydroxycholecalciferol are ineffective. Since 1,25-dihydroxycholecalciferol is synthesized in the kidney, these findings, in conjunction with the current study, are consistent with the association of experimental diabetes with a renal defect depressing synthesis of 1,25-dihydroxycholecalciferol. Since insulin treatment restores duodenal Ca transport, the renal defect is probably not caused by streptozotocin nephrotoxicity.