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Dadun > Depósito Académico > CIMA (Centro de Investigación Médica Aplicada) > Área de Terapia génica y Hepatología > Hepatología experimental > DA - CIMA - Terapia génica y Hepatología - Hepatología experimental - Artículos de revista >

Insulin-like growth factor I improves intestinal barrier function in cirrhotic rats
Authors: Lorenzo-Zuñiga, V. (V.)
Rodriguez-Ortigosa, C.M. (Carlos M.)
Bartoli, R. (R.)
Martinez-Chantar, M.L. (María Luz)
Martinez-Peralta, L. (L.)
Pardo, A. (A.)
Ojanguren, I. (I.)
Quiroga, J. (Jorge)
Planas, R. (R.)
Prieto, J. (Jesús)
Keywords: Insulin-Like Growth Factor I/therapeutic use
Intestinal Absorption/drug effects
Liver Cirrhosis, Experimental/drug therapy
Issue Date: 2006
Publisher: BMJ Publishing Group
Publisher version: http://gut.bmj.com/content/55/9/1306
ISSN: 1468-3288
Citation: Lorenzo-Zuniga V, Rodriguez-Ortigosa CM, Bartoli R, Martinez-Chantar ML, Martinez-Peralta L, Pardo A, et al. Insulin-like growth factor I improves intestinal barrier function in cirrhotic rats. Gut 2006 Sep;55(9):1306-1312.
Abstract
BACKGROUND AND AIMS: In liver cirrhosis, disruption of the intestinal barrier facilitates bacterial translocation and spontaneous bacterial peritonitis. Insulin-like growth factor I (IGF-I) is an anabolic hormone synthesised by hepatocytes that displays hepatoprotective activities and trophic effects on the intestine. The aim of this study was to investigate the effect of IGF-I on intestinal barrier function in cirrhotic rats. METHODS: In rats with carbon tetrachloride induced cirrhosis, we investigated the effect of IGF-I therapy on: (a) portal pressure; (b) intestinal histology and permeability to endotoxin and bacteria; (c) intestinal expression of cyclooxygenase 2 (COX-2) and tumour necrosis factor alpha (TNF-alpha), two factors that influence in a positive and negative manner, respectively, the integrity of the intestinal barrier; (d) intestinal permeability to 3H-mannitol in rats with bile duct ligation (BDL); and (e) transepithelial electrical resistance (TER) of polarised monolayers of rat small intestine epithelial cells. RESULTS: IGF-I therapy reduced liver collagen expression and portal pressure in cirrhotic rats, induced improvement in intestinal histology, and caused a reduction in bacterial translocation and endotoxaemia. These changes were associated with diminished TNF-alpha expression and elevated COX-2 levels in the intestine. IGF-I reduced intestinal permeability in BDL rats and enhanced barrier function of the monolayers of epithelial intestinal cells where lipopolysaccharide (LPS) caused a decrease in TER that was reversed by IGF-I. This effect of IGF-I was associated with upregulation of COX-2 in LPS treated enterocytes. CONCLUSIONS: IGF-I enhances intestinal barrier function and reduces endotoxaemia and bacterial translocation in cirrhotic rats. IGF-I therapy might be useful in the prevention of spontaneous bacterial peritonitis in liver cirrhosis.
Permanent link: http://hdl.handle.net/10171/23286
Appears in Collections:DA - CUN - Hepatología - Artículos de revista
DA - CIMA - Terapia génica y Hepatología - Hepatología experimental - Artículos de revista

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