Nitric Oxide Synthase in Pancreatic Islets / Libristo.pl
Nitric Oxide Synthase in Pancreatic Islets

Kod: 06820790

Nitric Oxide Synthase in Pancreatic Islets

Autor Saleem Saaed Qader

The influences of trauma and TPN on pancreatic islet §hormone secretion in relation to islet expression of §iNOS synthase was investigated.§§Acute pancreatitis resulted in an impaired glucose-§stimulated insulin secretion (GSIS), ... więcej

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Opis

The influences of trauma and TPN on pancreatic islet §hormone secretion in relation to islet expression of §iNOS synthase was investigated.§§Acute pancreatitis resulted in an impaired glucose-§stimulated insulin secretion (GSIS), which was found §to be parallelled by a marked expression of iNOS and §an exaggerated NO production in the pancreatic §islets. §A characteristic feature of long term TPN-treatment §is hyperlipidemia and euglycaemia. TPN treatment §impairs GSIS at least in part through a reduced §cyclic AMP production in parallell with an exclusive §expression of iNOS, which was reflected in an §increased NO production accompanied by enhanced §cyclic GMP formation by islets. §Agents stimulating cyclic AMP/PKA i.e. PACAP27 and §PACAP38 were capable of not only inhibiting neuronal §NOS (ncNOS) but also counteracting the expression of §iNOS induced by intralipid infusion. The suppressed §NO production in the presence of PACAPs was §reflected in a suppressed cyclic GMP and a marked §increase in cyclic AMP production by pancreatic §islets. §Finally, effects of ghrelin on islet hormone §secretion and NOS isoenzymes activities were also §studied. The influences of trauma and TPN on pancreatic islet hormone secretion in relation to islet expression of iNOS synthase was investigated. Acute pancreatitis resulted in an impaired glucose- stimulated insulin secretion (GSIS), which was found to be parallelled by a marked expression of iNOS and an exaggerated NO production in the pancreatic islets. A characteristic feature of long term TPN-treatment is hyperlipidemia and euglycaemia. TPN treatment impairs GSIS at least in part through a reduced cyclic AMP production in parallell with an exclusive expression of iNOS, which was reflected in an increased NO production accompanied by enhanced cyclic GMP formation by islets. Agents stimulating cyclic AMP/PKA i.e. PACAP27 and PACAP38 were capable of not only inhibiting neuronal NOS (ncNOS) but also counteracting the expression of iNOS induced by intralipid infusion. The suppressed NO production in the presence of PACAPs was reflected in a suppressed cyclic GMP and a marked increase in cyclic AMP production by pancreatic islets. Finally, effects of ghrelin on islet hormone secretion and NOS isoenzymes activities were also studied.

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309.36

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