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Functional and Metabolic Changes in Intestinal Mucosa of Rats After Enteral Administration of Ornithine α‐Ketoglutarate Salt
Author(s) -
Raul Francis,
Gosse Francine,
Galluser Michel,
Hasselmann Michel,
Seiler Nikolaus
Publication year - 1995
Publication title -
journal of parenteral and enteral nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.935
H-Index - 98
eISSN - 1941-2444
pISSN - 0148-6071
DOI - 10.1177/0148607195019002145
Subject(s) - ornithine , transamination , putrescine , diamine oxidase , intestinal mucosa , ornithine decarboxylase , enteral administration , biochemistry , ornithine carbamoyltransferase , medicine , chemistry , biology , endocrinology , amino acid , arginine , enzyme , parenteral nutrition
Background: Ornithine α‐ketoglutarate salt efficiently improves the nutritional status of protein‐depleted patients. Our aim was to explore the effects of ornithine α‐ketoglutarate supplementation on intestinal physiology in healthy animals. Methods: Rats were given a nutritive mixture supplemented with ornithine α‐ketoglutarate (1 g·kg −1 per day) by enteral route for 7 days. Controls received the diet supplemented with casein acid hydrolysate under isoenergetic and isonitrogenous conditions. Results: An adaptive hyperplasia of the villi and an increase in the brush‐border hydrolase activities were observed in rats receiving ornithine α‐ketoglutarate. Because of the high ornithine aminotransferase activity, ornithine α‐ketoglutarate‐derived ornithine was extensively transaminated with a concomitant enhancement of ornithine decarboxylation. Surprisingly, with glutamate and putrescine, the products of ornithine transamination and decarboxylation, γ‐aminobutyric acid accumulated (10‐fold to 16‐fold) dramatically in the intestinal mucosa of rats treated with ornithine α‐ketoglutarate. Because γ‐aminobutyric acid formation was completely prevented by the diamine oxidase inhibitor aminoguanidine but was not modified after inactivation of ornithine aminotransferase by 5‐fluoromethylornithine, it is evident that γ‐aminobutyric acid is formed in the mucosa from ornithine via putrescine as an intermediate. Conclusions: It is assumed that enhanced γ‐aminobutyric acid formation in the intestinal mucosa by ornithine α‐ketoglutarate treatment might be of physiologic importance in the regulatory processes of cell growth and differentiation. ( Journal of Parenteral and Enteral Nutrition 19: 145–150, 1995)