Glucose stimulates and insulin inhibits release of pancreatic TRH in vitro

Objective: Pancreatic TRH is present in insulin-producing B-cells of the is lets of Langerhans. There is fragmentary evidence that it may be involved i n glucoregulation, The aim of our present study was to analyze how glucose and insulin affect TRH secretion by the pancreatic islets. Design: Isolated pancreatic islets were incubated with different concentrat ions of glucose, insulin and glucagon, and TRH release was measured. Results: In the present study, 6 and 12 mmol/l D-glucose caused significant TRH release from isolated adult rat pancreatic islets when compared with t hat in the presence of the same concentrations of biologically ineffective L-glucose. Thirty mmol/l D-glucose was also ineffective, but this was not d ue to depression of secretion by hyperosmolarity since isosmotic compensati on for the high glucose addition did not restore its stimulatory effect, Fi ve mu mol/l dibutyryl cyclic 3',5'-adenosine monophosphate (db-cAMP) increa sed both basal and glucose-stimulated TRH release, but this effect was not seen with 50 mu mol/l db-cAMP. Stimulation of phosphodiesterase by imidazol e resulted in decreased basal but not glucose-stimulated release of TRH. Gl ucagon (10(-7) mol/l) did not affect either basal or glucose-stimulated rel ease of TRH, while insulin (10(-7) and 10(-6) mol/l) inhibited both, Conclusion: Our present data showing that glucose stimulates and insulin in hibits pancreatic TRH release are compatible with the possibility that this substance may play a role in glucoregulation.