Intestinal zinc transport: influence of streptozotocin-induced diabetes, insulin and arachidonic acid

The influence of arachidonic acid (AA) on the zinc flux rates of jejunal segments, isolated from streptozotocin-induced diabetic rats injected with saline or with insulin, was investigated using an Ussing chamber technique. Although the zinc flux rates from mucosa-to-serosa (Jms) of normal rats were inhibited by addition of 5 microM AA to the jejunal segment bathing medium (46.4 +/- 5.0 vs 32.6 +/- 4.3 nmol/hr/cm2), AA had no effect on the Jms of diabetic rats either with or without insulin treatment. Induction of diabetes also significantly reduced Jms (46.4 +/- 5.0 vs 22.1 +/- 4.9 nmol/hr/cm2), but 3 day insulin treatment (NPH 8 U/Kg/day subcutaneously) did not reverse this effect (29.2 +/- 5.1 nmol/hr/cm2). Addition of AA to the serosal side did not significantly alter the zinc flux rate from serosa-to-mucosa (Jsm) in either control, diabetic or diabetic rats treated with insulin. The net zinc absorption rate (Jnet) of jejunal segments was decreased in diabetic rats compared to controls (13.2 +/- 3.0 vs -0.7 +/- 2.1 nmol/hr/cm2), but normalization of blood glucose with 3 day insulin treatment did not increase Jnet. Addition of AA was associated with a tendency to increase zinc uptake capacity. This change reached statistical significance in insulin treated diabetic rats. Short-circuit current (Isc) for diabetic rats was increased compared to controls but addition of AA to the mucosal side bathing medium decreased Isc in all groups. The results indicate that the zinc flux rate in the small intestine of streptozotocin-induced diabetic rats is decreased, that zinc uptake capacity of the small intestine does not directly reflect the zinc flux rate across the small intestine, and that AA or one of its metabolites may play a significant role in the control of the zinc flux across the intestinal epithelium.