Intestinal Inflammation Increases Gastrointestinal Threonine Uptake and Mucin Synthesis in Enterally Fed Minipigs  

Oleh:

Remond, Didier ; Buffiere, Caroline ; Godin, Jean-Philippe ; Mirand, Philippe Patureau

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: JN: The Journal of Nutrition vol. 139 no. 04 (Apr. 2009), page 720-726.
Topik: Nutrient Requirements and Optimal Nutrition

Ketersediaan

Perpustakaan FK Nomor Panggil: J42.K.2009.02 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

The high requirement of the gut for threonine has often been ascribed to the synthesis of mucins, secreted threonine-rich glycoproteins protecting the intestinal epithelium from injury. This requirement could be even greater during intestinal inflammation, when mucin synthesis is enhanced. In this study, we used an animal model to investigate the effects of an acute ileitis on threonine splanchnic fluxes. Eight adult multi-catheterized minipigs were fed with an enteral solution. Four of them were subjected to experimental ileitis involving direct administration of trinitrobenzene sulfonic acid (TNBS) into the ileum (TNBS-treated group) and the other 4 were not treated (control group). Threonine fluxes across the portal-drained viscera (PDV) were quantified with the use of simultaneous i.g. L-[15N]threonine and i.v. L-[U-13C]threonine infusions. Ileal mucosa was sampled for mucin fractional synthesis rate measurement, which was greater in the TNBS-treated group (114 ± 15%/d) than in the control group (61 ± 8%/d) (P = 0.021). The first-pass extraction of dietary threonine by the PDV and liver did not differ between groups and accounted for 27 and 10% of the intragastric delivery, respectively. PDV uptake of arterial threonine increased from 25 ± 14 µmol•kg–1.h–1 in the control group to 171 ± 35 µmol•kg–1.h–1 in the TNBS-treated group (P < 0.001). In conclusion, ileitis increased intestinal mucin synthesis and PDV utilization of threonine from arterial but not luminal supply. This leads to the mobilization of endogenous proteins to meet the increased threonine demand associated with acute intestinal inflammation.

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