Maintaining adequate nutrition, not probiotic administration, prevents growth stunting and maintains skeletal muscle protein synthesis rates in a piglet model of colitis.
Malnutrition and cytokine-induced catabolism are pervasive in children with inflammatory bowel diseases (IBD), however, the benefits of aggressive nutrition support or of probiotics on nutrient and functional deficiencies and growth remain unclear. Piglets with dextran sulfate (DS)-induced colitis consuming a 50% macronutrient restricted diet (C-MR) were compared with those receiving probiotics (C-MRP) or adequate nutrition (C-WN) and with healthy well-nourished controls (REF). C-WN versus REF had reduced growth (-34% chest circumference and -22% snout-to-rump length gain) and a tendency toward lesser weight gain, but no differences in skeletal muscle protein fractional synthesis rates (FSR) or initiation of translation via the mTOR pathway were observed. Compared with C-WN, the C-MR and C-MRP piglets had lower weight gain, growth, and skeletal muscle FSR, and lower phosphorylated p70S6K1 with higher eIF4E*4E-BP1, indicative of reduced initiation of protein translation. Finally, plasma leucine concentrations were positively correlated with weight and phosphorylated p70S6K1, whereas negatively correlated with eIF4E*4E-BP1. In conclusion, reductions in weight gain, growth, protein turnover, skeletal muscle FSR, and initiation of protein translation with moderate macronutrient restriction in colitis are not ameliorated by probiotic supplementation. However, maintaining adequate nutrient intake during colitis preserves whole body protein metabolism, but growth remains compromised.
Harding
Scott V
SV
School of Dietetics and Human Nutrition, McGill University, Quebec, Canada.
Adegoke
Olasunkanmi A J
OA
Fraser
Keely G
KG
Marliss
Errol B
EB
Chevalier
Stéphanie
S
Kimball
Scot R
SR
Jefferson
Leonard S
LS
Wykes
Linda J
LJ
D000824:Animal Nutritional Physiological Phenomena; D000818:Animals; D000831:Animals, Newborn; D001786:Blood Glucose / Q000378:metabolism; D049628:Body Size; D003092:Colitis / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*; D016264:Dextran Sulfate; D004195:Disease Models, Animal; D004750:Enteral Nutrition; D039561:Eukaryotic Initiation Factor-4E / Q000378:metabolism; D006130:Growth Disorders / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D006854:Hydrocortisone / Q000097:blood; D007328:Insulin / Q000097:blood; D047908:Intracellular Signaling Peptides and Proteins / Q000378:metabolism; D007930:Leucine / Q000097:blood; D009124:Muscle Proteins / Q000096:biosynthesis*; D018482:Muscle, Skeletal / Q000378:metabolism*; D009752:Nutritional Status; D010766:Phosphorylation; D019936:Probiotics / Q000008:administration & dosage*; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D038762:Ribosomal Protein S6 Kinases, 70-kDa / Q000378:metabolism; D013552:Swine; D058570:TOR Serine-Threonine Kinases; D054875:Ubiquitination; D015430:Weight Gain
D001786:Blood Glucose; D039561:Eukaryotic Initiation Factor-4E; D007328:Insulin; D047908:Intracellular Signaling Peptides and Proteins; D009124:Muscle Proteins; D016264:Dextran Sulfate; C546842:MTOR protein, human; D017346:Protein Serine-Threonine Kinases; D051057:Proto-Oncogene Proteins c-akt; D038762:Ribosomal Protein S6 Kinases, 70-kDa; D058570:TOR Serine-Threonine Kinases; D007930:Leucine; D006854:Hydrocortisone