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 venou s and arterial, ruminal, and abomasal (steers) or duodenal (wethers) c atheters were used in two crossover design experiments to evaluate ada ptation 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 por tions and infused with an alpha-amylase partial starch hydrolysate (SH ) either postruminally (adapted) or ruminally (unadapted) for 4 (steer s; 40 g/h) or 5 (sheep; 6 g/h) days before measuring splanchnic flux o f metabolites. On the day of flux measurements, ruminal SH infusion wa s switched to the postruminal site in unadapted animals. Flux measurem ents 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 co transport, was then postruminally infused (550 and 500 mu mol/h for St eers and sheep, respectively) and flux measurements repeated from h 9 to 12 (steers) and h 7 to 10 (sheep). In the steers, adaptation increa sed (P less than or equal to 1.09) portal-drained visceral (PDV) gluco se release 26 mmol/h and decreased hepatic uptake of lactate 20 mmol/h . Abomasal infusion of phlorizin decreased (P = .01) net PDV glucose f lux 40 mmol/h and concomitantly increased (P = .05) hepatic release of glucose by 47 mmol/h. In sheep, duodenal infusion of phlorizin increa sed (P less than or equal to .005) portal and hepatic blood flow and d ecreased (P less than or equal to .02) PDV release of glucose and lact ate by 9 and .4 mmol/h, respectively. The liver released 4.2 mmol/h mo re (P = .09) glucose and removed 3.2 mmol/h more lactate (P = .001); a rterial 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 mainta in the Na/glucose cotransporter when consuming Little preformed alpha- glucosidic polymers and that the Liver increases glucose release to co mpensate for reduced PDV delivery of glucose to maintain glucose homeo stasis. In addition, the steers maintain at least 960 mmol/d and the s heep maintain at least 216 mmol/d of glucose transport capability rega rdless of adaptation. Steers (Exp. 1) adapted to luminal starch by del ivering more glucose to the liver, whereas sheep (Exp. 2) did not deli ver more glucose to the Liver and;may have increased visceral glucose utilization.