title: Increased tissue protein synthesis during spontaneous inflammatory bowel disease in HLA-B27 rats.
abstract: Inflammatory bowel diseases (IBDs) are associated with an increased whole-body protein turnover. In certain drug-induced experimental models of IBD, disturbances of protein synthesis in tissues have been reported recently, but it is unclear if similar disturbances occur in other chronic intestinal diseases. Therefore we investigated changes in protein synthesis in different tissues of HLA-B27 (human leucocyte antigen B27) transgenic rats that develop spontaneously chronic inflammation, with major involvement of the colon. Protein synthesis rate in HLA-B27 rats was shown to be higher in nine different tissues compared with control (Fisher 344) rats. The absolute rate of protein synthesis was highly stimulated at the main inflammatory site (+290% in the colon). However, liver, muscle and skin appeared to be major contributors to the increased protein synthesis observed at the whole-body level. Despite the increased protein synthesis, HLA-B27 rats presented a marked atrophy of muscles, which suggests an increased proteolysis. These results contrast with metabolic disturbances described in acute inflammation and colitis induced by drugs (i.e. dextran sodium sulphate). The present study suggests that the modifications of protein metabolism are strongly influenced by the type of the inflammatory diseases and thus by the underlying mechanisms, which result in different metabolic adaptations and specific nutritional requirements.
authors.affiliation: Unité de Nutrition et Métabolisme Protéique, Centre de Recherches INRA, 63122 Saint Genès Champanelle, France.
authors.forename: Mimoun
authors.initials: M
authors.lastname: El Yousfi
authors.forename: Denis
authors.initials: D
authors.lastname: Breuillé
authors.forename: Isabelle
authors.initials: I
authors.lastname: Papet
authors.forename: Stéphanie
authors.initials: S
authors.lastname: Blum
authors.forename: Marc
authors.initials: M
authors.lastname: André
authors.forename: Laurent
authors.initials: L
authors.lastname: Mosoni
authors.forename: Philippe
authors.initials: P
authors.lastname: Denis
authors.forename: Caroline
authors.initials: C
authors.lastname: Buffière
authors.forename: Christiane
authors.initials: C
authors.lastname: Obled
mesh_terms: D000208:Acute Disease; D000818:Animals; D030801:Animals, Genetically Modified; D001772:Blood Cell Count; D003106:Colon / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D015796:HLA-B27 Antigen / Q000235:genetics* / Q000276:immunology; D015212:Inflammatory Bowel Diseases / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D007413:Intestinal Mucosa / Q000276:immunology / Q000473:pathology; D008099:Liver / Q000378:metabolism; D008297:Male; D023421:Models, Animal; D018482:Muscle, Skeletal / Q000378:metabolism; D014176:Protein Biosynthesis; D051381:Rats; D011916:Rats, Inbred F344; D012867:Skin / Q000378:metabolism
chemical_list: D015796:HLA-B27 Antigen