Effect of abomasal glucose infusion on splanchnic and whole-body glucose metabolism in periparturient dairy cows

Abstract

Six periparturient Holstein cows fitted with ruminal cannulas and permanent indwelling catheters in the hepatic portal vein, hepatic vein, mesenteric vein, and an artery were used to study the effects of abomasal glucose infusion on splanchnic and whole-body glucose metabolism. The experimental design was a split plot, with cow as the whole plot, treatment as the whole-plot factor, and days in milk (DIM) as the subplot factor. Cows were assigned to 1 of 2 treatments: the control (no infusion) or infusion (1,500 g/d of glucose infused into the abomasum from the day of calving). Cows were sampled at 12 d prepartum and at 4, 15, and 29 DIM. To study portal-drained visceral uptake of arterial glucose, [U-(13)C]glucose was continuously infused into the jugular vein on sampling days. Postpartum, voluntary dry matter intake and milk yield increased at a lower rate with the infusion compared with the control. The net portal flux of glucose increased with the infusion compared with the control, and 67 +/- 5% of the infused glucose was recovered as increased portal flux of glucose. The net hepatic flux of glucose was lower with the infusion compared with the control; however, the net hepatic flux of glucose per kilogram of dry matter intake was not affected by treatment. The arterial concentrations of glucose and insulin decreased and concentrations of nonesterified fatty acids increased from prepartum to 4 DIM with the control, but these effects were not observed with the infusion. The arterial concentration of beta-hydroxybutyrate decreased more from prepartum to 4 DIM with the infusion, compared with the control. Uptake of arterial [U-(13)C]glucose in the portal-drained viscera was affected neither by the infusion nor by the DIM and averaged 2.5 +/- 0.2%. The whole-body glucose supply changed to be less dependent on the recycling of lactate (Cori cycle) with the infusion. It was concluded that small intestinal glucose absorption is an efficient source of glucose to the peripheral tissues of dairy cows in very early lactation. At least 67% of the available glucose was recovered in the portal vein without affecting hepatic gluconeogenesis. Infused cows produced less milk and had a lower feed intake, indicating that an improved glucogenic status in very early lactation impaired metabolic adaptations to lactation.

Carbohydrate quantitative digestion and absorption in ruminants: from feed starch and fibre to nutrients available for tissues

“…The 'lost' glucose may be attributed to metabolism of glucose within the small intestine to supply glycerol for the absorption of long-chain fatty acids, as suggested by . It may also be partly due to residual microbial fermentation of glucose after hydrolysis of starch in the small intestine, as suggested by Larsen and Kristensen (2007). The contribution of arterial glucose to lactate net portal release remains unclear.…”

“…Given the high increased use of arterial glucose by PDV, the apparent portal (or mesenteric) recovery of glucose is thus underestimated when expressed as a net basis; it is substantially increased when changes in arterial uptake by PDV are taken into account but remains incomplete (from 51% to 71%; . Based on calculation of the area under the curve of net portal (or mesenteric) fluxes of glucose against time following a starchy meal in sheep (Ré mond et al, 2009) or an abomasal pulse of glucose in dairy cow (Larsen and Kristensen, 2007), first pass recovery of glucose may be almost complete. The 'lost' glucose may be attributed to metabolism of glucose within the small intestine to supply glycerol for the absorption of long-chain fatty acids, as suggested by .…”

Precursors for liver gluconeogenesis in periparturient dairy cows

“…The data presented in Table 1 for Larsen and Kristensen (2009b) are based on pAH analysis after deacetylation, whereas the published nutrient fluxes were not. Hence, total liver balances of glucogenic carbon for the control treatment were originally observed to be 80%, 90%, 73% and 75% at 214, 14, 115 and 129 days relative to parturition, respectively, as compared with 87%, 99%, 88% and 84% with nutrient fluxes based on deacetylated pAH (Table 1).…”

“…The consequence of overestimating liver glucose release and underestimating liver precursor uptake can be elucidated by comparison of total liver balance of glucogenic carbon, published by Kristensen (2009a and2009b), with the data presented from that study in Table1. The data presented in Table 1 for Larsen and Kristensen (2009b) are based on pAH analysis after deacetylation, whereas the published nutrient fluxes were not.…”

“…Data selection and analysis As can be noted in Table 1, it is only in the studies by Larsen and Kristensen (2009b), Raun and Kristensen (2011) and Larsen and Kristensen (2012) that all major potential precursors, including AAs, for liver gluconeogenesis have been determined concomitantly. Hence, these data were compiled to investigate the dynamics of precursor supply for liver gluconeogenesis in the periparturient period.…”