On gluconeogenesis of human liver. Accelerated hepatic glucose formation induced by increased precursor supply.
In 8 subjects in whom portal vein catheters had been inserted 5-6 days previously during cholecystectomy, arterial and portal concentrations of glucose, lactate, pyruvate, glycerol, alanine, free fatty acids, beta-hydroxybutyrate and acetoacetate revealed no significant differences. This provided the basis for the calculation of hepatic balances from arterio-hepatic venous substrate-differences in 17 healthy volunteers. In eight of them metabolic balances were determined during elevated hepatic lactate supply. Kinetics of the substrates throughout the whole test period in 9 controls showed no gross interference from the catheterization or infusion procedure. The elevated hepatic lactate concentration caused a doubling of hepatic glucose output, which could almost entirely be accounted for by a fivefold increase of hepatic lactate uptake. This acceleration of hepatic gluconeogenesis was accompanied by a significant increment of hepatic free fatty acid uptake, whereas hepatic ketone body production did not change. These data seem to support the view that hepatic energy requirements caused by an accelerated gluconeogenesis might be covered from enhanced free fatty acid oxidation.
D000328:Adult; D000409:Alanine / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005943:Gluconeogenesis; D005990:Glycerol / Q000378:metabolism; D006801:Humans; D007657:Ketone Bodies / Q000096:biosynthesis; D007773:Lactates / Q000378:metabolism; D008099:Liver / Q000378:metabolism*; D011773:Pyruvates / Q000378:metabolism
D005230:Fatty Acids, Nonesterified; D007657:Ketone Bodies; D007773:Lactates; D011773:Pyruvates; D000409:Alanine; D005990:Glycerol