Ca2+ participates in the stimulation of hepatic gluconeogenesis by glucagon and there is evidence that Ca2+ fluxes are modified in arthritic rats. These findings raise the question whether hepatic gluconeogenesis in arthritic rats responds differently to glucagon and Ca2+. The experimental system was the isolated perfused rat liver. In the presence of Ca2+, stimulation of hepatic gluconeogenesis by glucagon in arthritic rats was equal to that in normal rats in absolute terms, but higher in relative terms (104.5 and 45.2%, respectively). In the absence of Ca2+, however, stimulation of hepatic gluconeogenesis by glucagon in arthritic rats was smaller in both absolute and relative terms (18.5 and 41.9%, respectively). It can be concluded that the Ca2+-dependent component of gluconeogenesis activation by glucagon is more important in arthritic than in normal rats.
Arthritis; liver; gluconeogenesis; glucagon
