Dickerson Roland N, Karwoski Claudia B
Department of Pharmacy, The University of Tennessee Health Sciences Center, Memphis 38163, USA.
J Am Coll Nutr. 2002 Aug;21(4):351-6. doi: 10.1080/07315724.2002.10719234.
To assess the effect of endotoxemia on hepatic lipid content during parenteral nutrition (PN) in rats.
Twenty male Sprague-Dawley rats (185-230 gm) were randomized to receive PN (n=9) or PN plus a continuous infusion of E. coli 026:B6 lipopolysaccharide (LPS; n= 11). All animals received isocaloric (170 kcal/kg/day), isonitrogenous (1.1 g N/kg/day), glucose-based PN for the next 78 hours. After 30 hours of adaptation to TPN, the animals were randomized to receive PN or PN plus LPS at 6 mg/kg/day for the remaining 48 hours of study. The animals were euthanized and the livers were harvested.
Liver weight increased significantly (by 60%) from 7.5+/-0.6 g to 12.1+/-2.4 g (p < or = 0.01) in the animals who received PN versus LPS, respectively. The proportion of liver water remained the same for PN and LPS groups (72.9+/-3.2% versus 72.3+/-3.8%, respectively, p = N.S.). However, liver fat increased disproportionately (by about 130%) from 0.20+/-0.05 g to 0.46+/-0.20 g (p < or = 0.01) total fat weight or from 9.6+/-1.8% to 13.6+/-4.1% (p < or = 0.02) lipid content (g/g) of the dry liver weight for the PN and LPS groups, respectively.
Endotoxin, when given concomitantly with parenteral nutrition, increases hepatic lipid accumulation and thus augments the development of parenteral nutrition-associated fatty liver in rats.
评估内毒素血症对大鼠肠外营养(PN)期间肝脏脂质含量的影响。
将20只雄性Sprague-Dawley大鼠(体重185 - 230克)随机分为两组,一组接受PN(n = 9),另一组接受PN并持续输注大肠杆菌026:B6脂多糖(LPS;n = 11)。在接下来的78小时内,所有动物均接受等热量(170千卡/千克/天)、等氮量(1.1克氮/千克/天)的基于葡萄糖的PN。在适应全胃肠外营养30小时后,将动物随机分为两组,在研究的剩余48小时内,一组接受PN,另一组接受PN加6毫克/千克/天的LPS。动物处死后,取出肝脏。
接受PN和LPS的动物肝脏重量分别从7.5±0.6克显著增加至12.1±2.4克(增加了60%,p≤0.01)。PN组和LPS组肝脏水分比例保持不变(分别为72.9±3.2%和72.3±3.8%,p = 无统计学差异)。然而,肝脏脂肪不成比例地增加(约130%),PN组和LPS组总脂肪重量分别从0.20±0.05克增加至0.46±0.20克(p≤0.01),或肝脏干重的脂质含量分别从9.6±1.8%增加至13.6±4.1%(p≤0.02)。
内毒素与肠外营养同时给予时,会增加肝脏脂质蓄积,从而加剧大鼠肠外营养相关脂肪肝的发展。