Evidence for metabolic regulation of pancreatic glucagon secretion by XXXX .

@entity1160 @entity19 @entity9640 @entity840 @entity3839 @entity413 @entity855
To investigate effects by @entity9640 on pancreatic A-cell secretion and intermediary metabolism, isolated pancreatic islets from normal and @entity3839 treated @entity840 (A-cell rich islets) were incubated in the presence of @entity413 (5.5 mM) +/- @entity9640 (10 mM). @entity1160 significantly enhanced glucagon release from 297 +/- 54 to 528 +/- 53 pg/micrograms DNA/h in normal islets and from 553 +/- 31 to 806 +/- 50 pg/micrograms DNA/h in A-cell rich islets. All results were expressed on the basis of islet DNA concentration, being 66 +/- 4 ng DNA per normal islet and @entity19 ng DNA per A-cell rich islet. Simultaneously, @entity1160 suppressed @entity413 oxidation to 64 per cent in normal islets and to 47 per cent of basal oxidation in A-cell rich islets. Islet content of @entity855 was also reduced by @entity1160 to about 60 per cent in A-cell rich islets, but not significantly changed in normal islets. @entity1160 oxidation, at 5.5 mM- @entity413 , was considerably higher in A-cell rich islets (911 +/- 65 pmol/micrograms DNA/h) than in normal islets (313 +/- 52 pmol/micrograms DNA/h). Addition of porcine insulin (25 mU/ml) counteracted these effects by @entity1160 , i.e. suppressed glucagon release but increased @entity413 oxidation and @entity855 content of the A-cell rich islets. The present findings demonstrate that @entity1160 stimulates glucagon release and is readily metabolized by the A-cells. Furthermore, the regulation of glucagon secretion by @entity1160 appears to be reciprocally related to factors affecting @entity413 metabolism and @entity855 -levels in the A-cell.
