NITRIC OXIDE SYNTHASE IN PANCREATIC ISLETS
DURING TRAUMA AND PARENTERAL FEEDING
Versandkostenfrei!
Versandfertig in 6-10 Tagen
45,99 €
inkl. MwSt.
PAYBACK Punkte
23 °P sammeln!
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 inc...
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.
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.
Andere Kunden interessierten sich für
