BACKGROUND: Patients with liver cirrhosis have disturbances in the insulin-like growth factor I (IGF-I) system that favour insulin resistance and catabolism. High morbidity and mortality of such patients from infections may be related to further aggravation of this problem but human data are controversial. Here, the effect of lipopolysaccharide (LPS) endotoxin on the IGF system was studied in rats with cirrhosis. MATERIALS AND METHODS: One month after induction of cirrhosis by bile duct ligation, LPS was administered (0.5 mg/kg) and the IGF system assessed 24 h later. Sham-operated animals acted as controls. Circulating and liver mRNA of IGF-I and its binding proteins (IGFBPs) were measured. RESULTS: LPS reduced IGF-I and IGFBP-3 by 20% in the cirrhosis group. LPS induced insulin resistance (HOMA) in both groups. CONCLUSION: Our results show that LPS administered to cirrhotic rats induced changes in the IGF system that facilitate catabolism. This may be of importance for the accelerated tissue loss during infection and the acute phase response in liver cirrhosis.
BACKGROUND:Patients with liver cirrhosis have disturbances in the insulin-like growth factor I (IGF-I) system that favour insulin resistance and catabolism. High morbidity and mortality of such patients from infections may be related to further aggravation of this problem but human data are controversial. Here, the effect of lipopolysaccharide (LPS) endotoxin on the IGF system was studied in rats with cirrhosis. MATERIALS AND METHODS: One month after induction of cirrhosis by bile duct ligation, LPS was administered (0.5 mg/kg) and the IGF system assessed 24 h later. Sham-operated animals acted as controls. Circulating and liver mRNA of IGF-I and its binding proteins (IGFBPs) were measured. RESULTS: LPS reduced IGF-I and IGFBP-3 by 20% in the cirrhosis group. LPS induced insulin resistance (HOMA) in both groups. CONCLUSION: Our results show that LPS administered to cirrhotic rats induced changes in the IGF system that facilitate catabolism. This may be of importance for the accelerated tissue loss during infection and the acute phase response in liver cirrhosis.