title: Growth failure occurs through a decrease in insulin-like growth factor 1 which is independent of undernutrition in a rat model of colitis.
abstract: BACKGROUND
  Linear growth retardation is a frequent complication of inflammatory bowel disease in children. The precise mechanisms causing growth failure are not known.
  
  
  OBJECTIVE
  To determine the relative contribution of reduced calorie intake and inflammation to linear growth delay and to determine the effect of inflammation on the hypothalamic-pituitary-growth axis.
  
  
  METHODS
  Linear growth was assessed in prepubertal rats with trinitrobenzenesulphonic acid (TNBS) induced colitis, in healthy free feeding controls, and in a pair-fed group (i.e. healthy animals whose daily food intake was matched to the colitic group thereby distinguishing between the effects of undernutrition and inflammation).
  
  
  RESULTS
  Changes in length over five days in the TNBS colitis and pair-fed groups were 30% and 56%, respectively, of healthy free feeding controls. Linear growth was significantly reduced in the colitic group compared with the pair-fed group. Nutritional supplementation in the colitic group increased weight gain to control values but did not completely reverse the growth deficit. Plasma interleukin 6 (IL-6) concentrations were sixfold higher in the colitic group compared with controls. Plasma concentrations of insulin-like growth factor 1 (IGF-1) but not growth hormone (GH) were significantly lower in the colitic compared with the pair-fed group. Administration of IGF-1 to the colitic group increased plasma IGF-1 concentrations and linear growth by approximately 44-60%.
  
  
  CONCLUSIONS
  It seems likely that approximately 30-40% of linear growth impairment in experimental colitis occurs as a direct result of the inflammatory process which is independent of undernutrition. Inflammation acts principally at the hepatocyte/IGF-1 level to impair linear growth. Optimal growth in intestinal inflammation may only be achieved by a combination of nutritional intervention and anticytokine treatment.
authors.affiliation: Digestive Diseases Research Centre, St Bartholomew's and The Royal London School of Medicine and Dentistry, London, UK. A.B.Ballinger@mds.qmw.ac.uk
authors.forename: A B
authors.initials: AB
authors.lastname: Ballinger
authors.forename: O
authors.initials: O
authors.lastname: Azooz
authors.forename: T
authors.initials: T
authors.lastname: El-Haj
authors.forename: S
authors.initials: S
authors.lastname: Poole
authors.forename: M J
authors.initials: MJ
authors.lastname: Farthing
mesh_terms: D000818:Animals; D003092:Colitis / Q000139:chemically induced / Q000150:complications* / Q000503:physiopathology; D019587:Dietary Supplements; D005260:Female; D006130:Growth Disorders / Q000209:etiology* / Q000378:metabolism; D007334:Insulin-Like Growth Factor I / Q000037:antagonists & inhibitors*; D015850:Interleukin-6 / Q000378:metabolism; D008297:Male; D009748:Nutrition Disorders / Q000150:complications* / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar; D014302:Trinitrobenzenesulfonic Acid; D015430:Weight Gain / Q000502:physiology
chemical_list: D015850:Interleukin-6; D007334:Insulin-Like Growth Factor I; D014302:Trinitrobenzenesulfonic Acid