Effect of Prolonged Lithium Ingestion on Glucagon and Parathyroid Hormone Responses in Rats

Abstract

In the present study the hypothesis is tested that long‐term lithium administration produces a general lowering of hormone responses that are mediated via the adenyl cyclase‐cyclic AMP systems. Rats were given lithium in the food for more than one month before the experiments, and the serum lithium concentration was maintained at a level of 0.7–0.9 mM. Lithium administration did not lower the response to 33 or 100 U/kg b.wt. of parathyroid hormone as measured by the decrease in the urinary excretion of calcium and by an increase in urinary excretion of phosphate and cyclic AMP; on the contrary, the effects of parathyroid hormone were higher in the lithium than in the control group. Lithium did not lower the response to 200 μg/kg b.wt. glucagon as measured by liver glycogen breakdown. The liver glycogen concentration was equal in the lithium and in the control group before the hormone was administered; one hour after its administration the liver glycogen concentration was reduced by about 40 per cent in both groups. Lithium led to a significant increase in the response to glucagon as measured by the increase in the urinary excretion of cyclic AMP. On the basis of the data obtained the hypothesis under investigation must be rejected.

The Distribution of a Glucose Load in Lithium Treated Rats

“…1970). Long term lithium administration has been found to increase (Krulik & Zvolskf 1970) or not to influence liver glycogen (Olesen & Thomsen 1974). DeFeudis (1971) reported that lithium administration caused more radioactivity in the liver when a tracer dose of glucose had been administered.…”