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   <subfield code="a">Plasma concentrations of glucagon during hyperglycemic clamp with or without somatostatin infusion in obese subjects</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Enzo Bonora, Paolo Moghetti, Vittorio Cacciatori, Marina Zenere, Flavia Tosi, Daniela Travia, Giacomo Zoppini, Laura Perobelli, Michele Muggeo]</subfield>
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   <subfield code="a">Summary: The aim of the present study was to evaluate whether the inhibitory effect on pancreatic A-cell exerted by hyperglycemic hyperinsulinemia and/or by somatostatin administration is impaired in human obesity. For this purpose plasma glucagon concentrations were measured in 8 obese and 8 nonobese nondiabetic subjects during a 4-h hyperglycemic clamp. Synthetic cyclic somatostatin-14 was infused at the rate of 2.5 nmol/min during the third hour of the study. Fasting plasma glucagon was higher in obese than in nonobese subjects (242±32vs 163±15 pg/ml, p&lt;0.05) (mean±SEM). In the last 20 min of the glucose infusion period preceding somatostatin administration (100-120 min of the study) plasma glucagon averaged 195±26 pg/ml in obese and 122±13 pg/ml in nonobese subjects (p&lt;0.05), with a reduction of 19±3% in the former and 28±4% in the latter (p=n.s.). In both groups somatostatin infusion did not result in a further decrease in plasma glucagon, which averaged 192±27 pg/ml in obese and 123±16 pg/ml in nonobese subjects (p&lt;0.05) in the 160-180 min period of the study. Also after discontinuing somatostatin infusion plasma glucagon levels did not change. These results suggest that in human obesity hyperglycemic hyperinsulinemia has a normal inhibitory effect on pancreatic A-cell and that somatostatin administration has no additive effect on hyperglycemia and hyperinsulinemia in either obese or nonobese nondiabetic subjects.</subfield>
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   <subfield code="a">Casa Editrice «il Ponte», 1990</subfield>
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   <subfield code="a">Glucagon</subfield>
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   <subfield code="t">Acta diabetologia latina</subfield>
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