The synthetase and dehydrogenase of prostaglandin (PG)D2 has been demonstrated in brain, spinal cord and alimentary tract, contrasting with those of PGE2 which has been previously investigated as a controller of endocrine pancreas. We examined the effect of PGD2 on pancreatic islet function in perfused rat pancreas.
Only glucagon was strongly released by 14μ M of PGD2 in the presence of 2.8mM glucose while both glucagon and insulin were released by 14μ M of PGE2. When 5.6mM glucose was used, result were same except the release of glucagon was partly diminished. The dose of PGD2 reduced to 1.4μ M, and glucagon release during 10 minutes was about one sixth of 14μ M PGD2 in the presence of 2.8mM glucose.
In conclusion, PGD2 released glucagon from perfused rat pancreas without insulin release, while PGE2 did release both of insulin and glucagon. Considering the fact that suppression of endogenous PG by aspirin or indomethacin restores glucose tolerance in diabetics, PGD2 but PGE2 may be a controller of endocine pancreas.
