Contribution of liver nerves, glucagon, and XXXX to the glycaemic response to exercise in @entity35 .

@entity1063 @entity1425 @entity35 @entity1943 @entity1718 @entity413
The contribution of hepatic sympathetic innervation, glucagon and @entity1425 to the glycaemic response to exercise was investigated in @entity35 . Hepatically denervated (LDX) or sham operated (SHAM) @entity35 with permanent catheters were therefore submitted to swimming with or without infusion of @entity1943 in combination with adrenodemedullation. Blood samples were taken for measurements of blood @entity413 , plasma free @entity1718 (FFA), @entity1425 (A), @entity1063 (NA), insulin and glucagon. Liver denervation by itself did not influence @entity413 levels during exercise. Infusion of @entity1943 in SHAM animals, which inhibited the exercise-induced glucagon response, led to enhanced sympathoadrenal outflow (measured as plasma A and NA) and a reduced blood @entity413 during exercise, suggesting that glucagon serves as a powerful mediator of the glycaemic response during swimming. Infusion of @entity1943 in LDX animals failed to enhance plasma NA levels and led to a more pronounced reduction in blood @entity413 levels. This indicates that liver nerves do contribute to the glycaemic response to exercise when glucagon secretion is suppressed. Reduced blood @entity413 levels after adrenodemedullation revealed that adrenal A is another important mediator of the @entity413 response to exercise. Infusion of @entity1943 in adrenodemedullated SHAM or LDX animals was not accompanied with increased NA outflow, suggesting that adrenal A is necessary to allow the compensatory increased outflow of NA from sympathetic nerves. In conclusion, the study shows that pancreatic glucagon and adrenal A are the predominant factors influencing the glycaemic response to exercise, whereas a role of the sympathetic liver nerves becomes evident when glucagon secretion is suppressed.
