Hepatic glycogen in humans. II. Gluconeogenetic formation after oral and intravenous glucose

The amount of glycogen that is formed by gluconeogenetic pathways during glucose loading was quantitated in human subjects. Oral glucose loading was compared with its intravenous administration. Overnight-fasted subjects received a constant infusion or [3-3H]glucose and a marker for gluconeogenesis, [U-14C]lactate or sodium [14C]bicarbonate [14C]bicarbonate). An unlabeled glucose load was then administered. Postabsorptively, or after glucose infusion was terminated, a third tracer ([6-3H]glucose) infusion was initiated along with a three-step glucagon infusion. Without correcting for background stimulation of [14C]glucose production or for dilution of 14C with citric acid cycle carbon in the oxaloacetate pool, the amount of glycogen mobilized by the glucagon infusion that was produced by gluconeogenesis during oral glucose loading was 2.9 +/- 0.7 g calculated from [U-14C]-lactate incorporation and 7.4 +/- 1.3 g calculated using [14C]bicarbonate as a gluconeogenetic marker. During intravenous glucose administration the latter measurement also yielded 7.2 +/- 1.1 g. When the two corrections above are applied, the respective quantities became 5.3 +/- 1.7 g for [U-14C]lactate as tracer and 14.7 +/- 4.3 and 13.9 +/- 3.6 g for oral and intravenous glucose with [14C]bicarbonate as tracer (P less than 0.05, vs. [14C]-lactate as tracer). When [2-14C]acetate was infused, the same amount of label was incorporated into mobilized glycogen regardless of which route of glucose administration was used. Comparison with previous data also suggests that 14CO2 is a potentially useful marker for the gluconeogenetic process in vivo.