Control of hepatic gluconeogenesis: role of XXXX oxidation.

@entity2125 @entity6212 @entity844 @entity26 @entity6178 @entity35 @entity413 @entity2388
@entity6212 has been found to activate the gluconeogenic pathway in perfused isolated @entity35 liver. Whether a net increase in the production of @entity413 is observed is a function of the relative concentrations of the @entity413 precursor and the @entity844 . The kinetics of @entity6212 interaction with the gluconeogenic pathway are influenced by the rate changes induced by decreases in @entity2388 concentration as a result of the increased @entity2125 redox potential produced by the oxidation of @entity844 . Taking this into account, two distinct effects of @entity6212 were identified. The first is an increase in the Vmax even at the lowest (25 microM) concentration of the @entity844 tested. The second is a progressive decrease in [ @entity2388 ]0.5 as a function of @entity6212 concentration. The latter occurs at low (less than 0.1 mM), presumably physiological, @entity2388 concentrations, when its mitochondrial transport is limiting, indicating that this process must have been activated. The former is observable even at high (greater than 0.5 mM), supraphysiological, concentrations of @entity2388 , when its mitochondrial transport is not limiting, indicating that a distal step, presumably @entity2388 carboxylation, is activated. The action of @entity6212 in increasing gluconeogenesis has been found not to be related to a decreased flux through @entity2388 dehydrogenase, neither to changes in the @entity2125 redox potential nor to its ability to increase energy production. Actually, the @entity26 uptake induced by @entity6212 was largely accounted for by the production of @entity6178 body and the latter process was found to be independent of variations in energy demand.
