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MUCOSAL BIOLOGY

Intestinal renal metabolism of L-citrulline and L-arginine following enteral or parenteral infusion of L-alanyl-L-[2,¹⁵N]glutamine or L-[2,¹⁵N]glutamine in mice

¹Department of Surgery of the Vrije Universiteit University Medical Center, Amsterdam; and ²University of Maastricht and Nutrition and Toxicology Research Institute, Maastricht, The Netherlands

Submitted 24 January 2005 ; accepted in final form 25 May 2005

Previously, we observed increased plasma arginine (ARG) concentrations after glutamine (GLN)-enriched diets, in combination with clinical benefits. GLN delivers nitrogen for ARG synthesis, and the present study was designed to quantify the interorgan relationship of exogenous L-GLN or GLN dipeptide, by enteral or parenteral route, contributing to intestinal citrulline (CIT) and renal de novo ARG synthesis in mice. To study this, we used a multicatheterized mouse model with Swiss mice (n = 43) in the postabsorptive state. Stable isotopes were infused into the jugular vein or into the duodenum {per group either free L-[2,¹⁵N]GLN or dipeptide L-ALA-L-[2,¹⁵N]GLN, all with L-[ureido-¹³C-²H₂]CIT and L-[guanidino-¹⁵N₂-²H₂]ARG} to establish renal and intestinal ARG and CIT metabolism. Blood flow was measured using ¹⁴C-para-aminohippuric acid. Net intestinal CIT release, renal uptake of CIT, and net renal ARG efflux was found, as assessed by arteriovenous flux measurements. Quantitatively, more de novo L-[2,¹⁵N]CIT was produced when free L-[2,¹⁵N]GLN was given than when L-ALA-L-[2,¹⁵N]GLN was given, whereas renal de novo L-[2,¹⁵N]ARG was similar in all groups. In conclusion, the intestinal-renal axis is hereby proven in mice in that L-[2,¹⁵N]GLN or dipeptide were both converted into de novo renal L-[2,¹⁵N]ARG; however, not all was derived from intestinal L-[2,¹⁵N]CIT production. In this model, the feeding route and form of GLN did not influence de novo renal ARG production derived from GLN.

intestines; kidney; metabolism

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