Abstract

Glucose utilization in isolated pancreatic islets of the rat was inhibited by prostaglandin (PG) E 2 and the α 2 adrenoceptor agonist, clonidine, to a similar extent; other prostaglandins did not affect glucose utilization. Islet oxidation of [1- 14C]glucose and [6- 14C]glucose demonstrated that the pentose phosphate shunt was inhibited by PGE 2 and clonidine. Pertussis toxin antagonizes the effects of clonidine and PGE 2 on total glucose utilization and pentose phosphate shunt activity. The results suggest that PGE 2 and α 2 adrenoceptor agonists may regulate glucose metabolism through similar transduction mechanisms, and that a guanine nucleotide binding regulatory (G) protein modulates certain metabolic effects of prostaglandins and adrenergic agonists.

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