Disposition of a mixed meal by the conscious dog

Abstract

The disposition of a mixed meal administered intragastrically was examined in 13 24-h-fasted conscious dogs, using the arteriovenous (AV) difference technique (and isotopic methods in 6 dogs). Postprandial net gut output totaled (in g of glucose equivalents) 42 +/- 6 glucose, 3 +/- 0.3 lactate, 2 +/- 0.2 alanine, and 0.2 +/- 0.0 glycerol. The gut oxidized 2 +/- 1 g of glucose, and 0.2 +/- 0.1 g remained within the intestinal lumen. Of the administered glucose 68 +/- 6% were accounted for, and volatile fatty acid production by the gut (n = 1) accounted for at least an additional 4%. Of the labeled glucose in the meal 82 +/- 5% appeared in the systemic circulation, an apparent overestimate of absorption of glucose from the meal. Cumulative net hepatic uptakes (in g of glucose equivalents) were 4.1 +/- 3.1 glucose, 12.1 +/- 2.1 gluconeogenic amino acids, and 1.5 +/- 0.2 glycerol. Net hepatic glycogen synthesis and lactate and CO2 production accounted for 6.2 +/- 4.1, 9.3 +/- 2.8, and 1.6 +/- 0.8 g of glucose equivalents, respectively. In summary, the AV difference method could account for the gut disposition of about two-thirds of the meal glucose. Nonsplanchnic tissues disposed of threefold more glucose than the liver. Net hepatic uptake of glucose equivalents as gluconeogenic amino acids was threefold > glucose uptake, and net hepatic uptake of gluconeogenic amino acids was > net gut release of gluconeogenic amino acids. In conclusion, the net hepatic uptake of glucose and gluconeogenic substrates provided adequate carbon for net hepatic synthesis of glycogen and production of lactate and CO2. In a net sense, peripheral tissues must have been the source of some of the gluconeogenic carbon taken up by the liver after the meal.

Route-dependent effect of nutritional support on liver glucose uptake

“…The lower arterial glucose levels likely contributed to the lower insulin levels. Consistent with previous studies, only ϳ70% of the glucose given enterally is absorbed as glucose (8,17); the remaining 30% is metabolized by the intestine. A failure to absorb 100% of the enterally delivered glucose as glucose is likely not the sole explanation for the lower insulin concentration in TPNϩEG.…”

Brain insulin action augments hepatic glycogen synthesis without suppressing glucose production or gluconeogenesis in dogs

“…Knowing that the insulinbrain-liver signaling axis was intact in dogs, we undertook a second set of experiments to determine whether a physiologic increase in brain insulin could activate central signaling and thereby modify hepatic glucose metabolism in vivo. To this end, we brought about an increase in brain insulin that was physiologic in both its route of administration (infused into the arteries that perfuse the brain) and its magnitude (~10-fold increase), the latter being within the physiologic range of arterial hyperinsulinemia seen after a mixed meal (26). In order to allow the impact of such a change to be clearly seen, we maintained basal insulin and glucagon levels at the liver.…”

Comparison of the time courses of insulin and the portal signal on hepatic glucose and glycogen metabolism in the conscious dog.

“…The liver is an important site of glucose removal after a meal (1,8,13,18,33,37,38). Several studies have demonstrated that the combination of hyperglycemia, hyperinsulinemia, and intraportal glucose infusion (portal signal) can produce rates of NHGU that are comparable with rates observed after glucose ingestion (32,39,40).…”