Diabetogenic effects of chronic oral cadmium adminstration to neonatal rats.
1 Chronic exposure of neonatal rats to oral cadmium (Cd) (0.1 and 1.0 micrograms/g daily for 45 days) disturbed glucose homeostasis, as reflected by hyperglycaemia, reduced liver glycogen and enhanced gluconeogenic potential of hepatic tissue. 2 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. 3 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. 4 The results are discussed in relation to the possible mechanism of the diabetogenic effect of Cd.
D000262:Adenylyl Cyclases / Q000378:metabolism; D000818:Animals; D000831:Animals, Newborn / Q000502:physiology*; D001786:Blood Glucose / Q000378:metabolism; D001806:Blood Urea Nitrogen; D002104:Cadmium / Q000633:toxicity*; D000242:Cyclic AMP / Q000096:biosynthesis; D003921:Diabetes Mellitus, Experimental / Q000139:chemically induced*; D005260:Female; D005943:Gluconeogenesis / Q000187:drug effects; D006128:Growth / Q000187:drug effects; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D008112:Liver Glycogen / Q000378:metabolism; D011247:Pregnancy; D051381:Rats
D001786:Blood Glucose; D007328:Insulin; D008112:Liver Glycogen; D002104:Cadmium; D000242:Cyclic AMP; D000262:Adenylyl Cyclases