Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022104 (irritable bowel syndrome)
 8,033 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hallmarks of IGF-I action include synergy with other hormones and growth factors and the ability to stimulate proliferation or differentiated cell function dependent on physiological or pathophysiologial context. A complete understanding of IGF action in IBD will require analyses of mechanisms of IGF interaction with other growth factors, hormones and cytokines. GH and IGF-I may be administered to children over prolonged periods to correct growth disorders. The definition of the benefits and problems of GH/IGF-I therapy in IBD needs to distinguish between long-term and short-term effects. Short-term administration of GH and IGF-I to animal models of IBD such as the PG-PS and TNBS models, which share features of Crohn's disease (Sartor, 1992), and a recently developed murine model of ulcerative colitis induced by ingestion of dextran sulphate (Okayasu et al, 1990; Sartor, 1992; Cooper et al, 1993) could address the beneficial or detrimental consequences of short-term GH/IGF-I therapy. Adaptation of the PG-PS, TNBS and dextran sulphate models of inflammation to available transgenic mouse lines that over-express GH and IGF-I (Behringer et al, 1990; Ulshen et al, 1993), especially if over-expression is inducible, could help to define the potential benefits and problems of long-term GH/IGF-I therapy or the effects of GH/IGF-I on immune cell function and cytokine production during intestinal inflammation. It will be useful to study intestinal inflammation and complication in animal models of GH or IGF-I deficiency. In this regard, mice with targeted ablation of the IGF-I gene could be useful (Liu et al, 1993) although neonatal mortality in these models currently poses problems for in vivo studies. Development of mesenchymal cell lines from such animals could, however, provide a useful in vitro system to study the role of IGF-I in altered cell function in response to pro-inflammatory cytokines.
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PMID:Insulin-like growth factors and inflammatory bowel disease. 873 2

In Japan, there is as yet no report on growth retardation in children with IBD. We therefore investigated the cause of growth retardation in Japanese children with IBD. We investigated the height, body weight, serum levels of albumin, IGF-I, CRP, and cytokines, and the amount of corticosteroid administered in children with Crohn's disease (CD, n = 15) and ulcerative colitis (UC, n = 18). Our results suggest that growth retardation is already present before the initial visit in children with CD, and chronic inflammation may be responsible this growth disturbance. Moreover, the amount of PSL used may contribute to growth retardation by decreasing the serum levels of IGF-I in children with IBD.
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PMID:Assessment of Growth Disturbance in Japanese Children with IBD. 2045 71