Abstract
Glucose utilization in isolated pancreatic islets of the rat was inhibited by prostaglandin (PG) E2 and the α2 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 PGE2 and clonidine. Pertussis toxin antagonizes the effects of clonidine and PGE2 on total glucose utilization and pentose phosphate shunt activity. The results suggest that PGE2 and α2 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.
| Original language | English |
|---|---|
| Pages (from-to) | 354-358 |
| Number of pages | 5 |
| Journal | Archives of Biochemistry and Biophysics |
| Volume | 269 |
| Issue number | 1 |
| DOIs | |
| State | Published - Feb 15 1989 |
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