Adaptation to small intestinal starch assimilation and glucose transport in ruminants.

Four crossbred steers (380 +/- 6 kg) and seven Polypay wethers (40.3 +/- 6 kg) fitted with hepatic venous, hepatic portal, mesenteric venous and arterial, ruminal, and abomasal (steers) or duodenal (wethers) catheters were used in two crossover design experiments to evaluate adaptation to small intestinal starch and glucose transport. Steers were fed 8.6 kg/d and sheep were fed .9 kg/d of alfalfa hay in 12 equal portions and infused with an alpha-amylase partial starch hydrolysate (SH) either postruminally (adapted) or ruminally (unadapted) for 4 (steers; 40 g/h) or 5 (sheep; 6 g/h) days before measuring splanchnic flux of metabolites. On the day of flux measurements, ruminal SH infusion was switched to the postruminal site in unadapted animals. Flux measurements were made 3 to 6 h after switching infusion site for steers and 2 to 5 h for sheep. Phlorizin, a competitive inhibitor of Na/glucose cotransport, was then postruminally infused (550 and 500 mumol/h for steers and sheep, respectively) and flux measurements repeated from h 9 to 12 (steers) and h 7 to 10 (sheep). In the steers, adaptation increased (P < or = .09) portal-drained visceral (PDV) glucose release 26 mmol/h and decreased hepatic uptake of lactate 20 mmol/h. Abomasal infusion of phlorizin decreased (P = .01) net PDV glucose flux 40 mmol/h and concomitantly increased (P = .05) hepatic release of glucose by 47 mmol/h. In sheep, duodenal infusion of phlorizin increased (P < or = .005) portal and hepatic blood flow and decreased (P < or = .02) PDV release of glucose and lactate by 9 and .4 mmol/h, respectively. The liver released 4.2 mmol/h more (P = .09) glucose and removed 3.2 mmol/h more lactate (P = .09) glucose and removed 3.2 mmol/h more lactate (P = .001); arterial glucose decreased (P = .003) .75 mM in response to phlorizin. Phlorizin also caused loss of glucose in the urine of sheep (.09 mmol/h). Adaptation did not alter net splanchnic flux of glucose, lactate, oxygen, or alpha-amino N. These studies indicate that ruminants maintain the Na/glucose cotransporter when consuming little preformed alpha-glucosidic polymers and that the liver increases glucose release to compensate for reduced PDV delivery of glucose to maintain glucose homeostasis. In addition, the steers maintain at least 960 mmol/d and the sheep maintain at least 216 mmol/d of glucose transport capability regardless of adaptation.(ABSTRACT TRUNCATED AT 400 WORDS)