DIABETOGENIC EFFECTS OF CHRONIC ORAL CADMIUM ADMINISTRATION TO NEONATAL RATS

Chronic exposure of neonatal rats to oral cadmium (Cd) (0.1 and 1.0 μg/g daily for 45 days) disturbed glucose homeostasis, as reflected by hyperglycaemia, reduced liver glycogen and enhanced gluconeogenic potential of hepatic tissue. This Cd‐exposure regimen also increased hepatic cyclic adenosine 3′,5′‐monophosphate (cyclic AMP) which was accompanied by enhancement of basal, adrenaline and glucagon‐stimulated form(s) of adenylate cyclase. In order to assess the responsiveness of pancreatic beta cells to glucose, islets isolated from control as well as Cd‐exposed animals were incubated in vitro and their rate of insulin secretion determined. In the presence of glucose 0.5 mg/ml, there was no significant difference in the rate of insulin release. However, at higher glucose concentrations (1.5 and 3.0 mg/ml), the islets from Cd‐exposed rats released significantly less insulin than those of control animals. The results are discussed in relation to the possible mechanism of the diabetogenic effect of Cd. 1980 British Pharmacological Society