Thomsen Karen Louise, Nielsen Susanne Schouw, Grønbiek Henning, Flyvbjerg Allan, Vilstrup Hendrik
Department of Medicine V (Hepatology and Gastroenterology), Clinical Institute, Aarhus University Hospital, DK-8000 Aarhus C, Denmark.
In Vivo. 2008 Nov-Dec;22(6):655-61.
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.
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.
LPS reduced IGF-I and IGFBP-3 by 20% in the cirrhosis group. LPS induced insulin resistance (HOMA) in both groups.
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.
肝硬化患者存在胰岛素样生长因子I（IGF-I）系统紊乱，这有利于胰岛素抵抗和分解代谢。这类患者因感染导致的高发病率和高死亡率可能与该问题的进一步加重有关，但相关人体数据存在争议。在此，研究了脂多糖（LPS）内毒素对肝硬化大鼠IGF系统的影响。
通过胆管结扎诱导肝硬化一个月后，给予LPS（0.5mg/kg），并在24小时后评估IGF系统。假手术动物作为对照。测量循环血和肝脏中IGF-I及其结合蛋白（IGFBPs）的mRNA水平。
在肝硬化组中，LPS使IGF-I和IGFBP-3降低了20%。LPS在两组中均诱导了胰岛素抵抗（HOMA）。
我们的结果表明，给肝硬化大鼠注射LPS会诱导IGF系统发生变化，促进分解代谢。这对于肝硬化患者感染期间加速的组织损耗和急性期反应可能具有重要意义。
