Energy and nutrient utilization by the calf's gut

Abstract

Calf scours are caused by a variety of infectious agents. Oral rehydration therapy solutions are formulated with the objective of correcting dehydration and acidosis. Currently, oral rehydraton therapy does not promote gut healing in diarrheic calves. However, investigators are examining the role of nutrition in promoting gut healing. Previous work has shown that the amino acid glutamine is important in nitrogen transport between tissues and is an indispensable nutrient for rapidly dividing cells such as lymphocytes, fibroblasts and enterocytes. Small intestinal epithelial cells depend mainly on glutamine, glucose, and ketone bodies for their energy under normal physiological conditions. The oxidative substrate preferred by large intestinal epithelial cells appears to be butyrate, followed by acetate, glutamine, and glucose. Research shows that glutamine supplementation increases intestinal protein synthesis. This may be one of the mechanisms by which glutamine exerts its protective effect on gut integrity and mucosal barrier function during critical illness. However, questions concerning the optimum dose and route by which glutamine is to be administered have yet to be addressed.

A surgical model was developed to chronically study the nutrient concentration differences across the portal-drained viscera of preruminant calves. The experimental design consisted of a series of infusions conducted on four different study days in each calf. On the study days, 4 separate 1h infusions of acetate, glucose, glutamine, saline (control) were administered intravenously via the jugular vein at 200 mmol/L/h in a different order. Venous and arterial blood were collected over the last 15 min of each 1h infusion. Blood flow was also measured. Intestinal uptake in ìmol/kg0.75/min was 0.3 ± 1.1 for glutamine and 1.9 ± 3.1 for glucose during saline infusion. During acetate, glucose, and saline infusions, glucose was a greater source of energy than glutamine for the intestine. However, during glutamine infusion, intestinal glutamine uptake (29.9 ± 11.2 ìmol/kg0.75/min) increased significantly which was associated with a rise in ammonia production (7.0 ± 0.5 ìmol/kg0.75min). A second experiment was designed to determine if glutamine uptake could be further stimulated either by longer term intravenous infusion or by chronic oral supplementation in neonatal calves. Intestinal metabolism was investigated by measuring nutrient uptake during three intravenous infusions of glutamine over a 5 h period after an overnight fast. Prior to the first infusion, calves diet consisted of milk only. Diet was supplemented with oral glutamine for the second and third infusions. Glutamine was administered via the jugular vein at a rate of 200 mmol/L/h. Venous and arterial blood was collected in duplicate every hour for 5 h. Blood flow was also measured. During glutamine infusion, there was an absolute increase in PDV uptake of glutamine associated with a significant production of ammonia. Feeding glutamine orally did not alter the PDV glutamine uptake. Glutamine infusion did not increase the intestinal uptake of essential amino acids. Neither chronic oral supplementation with glutamine, or infusion for periods longer than an hour, further increased intestinal glutamine uptake. Arterial leucine concentration and intestinal uptake declined during glutamine infusion suggesting that its supply became limiting. Thus glutamine supplementation may require the provision of a mixture of amino acids to be effective.