Enteral ornithine alpha-ketoglutarate enhances intestinal adaptation to massive resection in rats.

Ornithine alpha-ketoglutarate (OKG) has been advocated in the treatment of critically ill patients for its anabolic effect on protein metabolism. Since OKG is a precursor of glutamine, arginine, and polyamines, key substrates of intestinal metabolism and function, we investigated the influence of OKG on intestinal adaptation and trophicity and on glutamine status after small bowel resection. After massive (80%) small bowel resection, rats were enterally fed for 7 days with a standard diet supplemented with either OKG (2 g/kg/d) or an isonitrogenous amount of glycine. OKG induced an adaptative hyperplasia of the villi, demonstrated in the jejunum by an increase in the villus height to crypt depth ratio (OKG v control, 4.3+/-0.4 v 3.3+/-0.5, P < .01) along with an increase (P < .05) in ornithine decarboxylase (ODC) activity (+80%) and ornithine content (+102%). Plasma glutamine (+25%) and muscle glutamine (anterior tibialis [AT], +43%; extensor digitorum longus [EDL], +54%) and protein (AT, +32%) were significantly higher (P < .05) after OKG administration, supporting its role in the restoration of glutamine pools. In summary, enterally administered OKG, which enhances intestinal adaptation after massive resection and improves muscle glutamine and protein content, could contribute significantly to nutritional management after small bowel resection.