A role for XXXX in cephalic phase of postprandial thermogenesis in @entity235 .

@entity4962 @entity9959 @entity235 @entity1425 @entity3897 @entity1063
The influence of @entity9959 in the cephalic phase of postprandial thermogenesis was investigated in @entity235 . O2 consumption (VO2) and respiratory quotient (RQ) were continuously monitored 1 h before and 2 h after a 1,015-kcal meal during a control, an @entity3897 , or a pancreatic-denervation experiment. A first phase (cephalic phase) in VO2 increase, lasting at least 50 min, followed by a second phase (digestive phase) were found in the control experiment. During both the @entity3897 and pancreatic-denervation experiment, the first phase of @entity4962 was inhibited by 52%. The second phase was completely abolished with @entity3897 , whereas it remained comparable to the control in the case of pancreatic denervation. A peak increase for @entity9959 time) was observed 2 min after the onset of feeding in control. It was followed after 25 min by a second increase related to changes in glycemia. Maximal rises of @entity1063 (NE) and @entity1425 corresponded to 215 and 120 pg/ml above basal values at 2 min in control experiment. During both @entity3897 and pancreatic denervation the cephalic phase of @entity9959 release was suppressed and the NE increase was inhibited by congruent to 65%. During the digestive phase pancreatic denervation caused an increase in plasma @entity9959 comparable to that of the control, whereas @entity3897 produced no such effect. It is suggested that the cephalic phase of postprandial thermogenesis is mediated through a causal relationship between @entity9959 and NE release.
