Impaired intestinal sugar transport in cirrhotic rats: correction by low doses of insulin-like growth factor I
Castilla-Cortazar I, Prieto J, Urdaneta E, Pascual M, Nuñez M, Zudaire E, Garcia M, Quiroga J, Santidrian S.
Department of Human Physiology, School of Medicine, University of Navarra, Pamplona, Spain
Date: Oct 1, 1997Hepatology
BACKGROUND & AIMS
Malnutrition is a complication of liver cirrhosis accompanied by reduced insulin-like growth factor I (IGF-I) availability. The aim of this study was to analyze the effect of IGF-I on intestinal D-galactose absorption in cirrhotic rats.
IGF-I (2 micrograms.100 g body wt-1.day-1) or saline were given for 14 days to rats in whom cirrhosis was induced with CCl4. Galactose transport and sodium-glucose/galactose-ligand transporter 1 (SGLT-1) expression were assessed in jejunal rings and in brush border membrane vesicles (BBMVs).
Compared with that in controls, galactose transport in everted jejunal rings was significantly reduced in cirrhotic rats but showed normal values after IGF-I treatment. The kinetic study of D-galactose uptake by BBMVs showed decreased maximal velocity (Vmax) and diminished transporter affinity in cirrhotic rats. These kinetic parameters reverted to normal after IGF-I treatment. Microvilli were significantly elongated in cirrhotic rats but of normal size in the IGF-I-treated group. The expression of SGLT-1 on BBMVs (Western blot) and on the luminal membrane of enterocytes (immunohistochemistry) was not reduced in cirrhotic animals compared with controls or IGF-treated cirrhotic rats.
Intestinal sugar transport is disturbed in experimental cirrhosis, and this alteration is corrected by IGF-I.
CITATION Gastroenterology. 1997 Oct;113(4):1180-7
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