Larsson-Backström C, Arrhenius E, Sagge K, Lindmark L, Paprocki J, Svensson L
Department of Experimental Biology, Kabi Nutrition, Stockholm, Sweden.
Circ Shock. 1990 Apr;30(4):331-47.
The sequential changes in lipid metabolism and in the fatty acid profile of liver lipids during fasting and sepsis were studied. Liver and blood specimens were taken from normally fed rats and from nonseptically and septically fasted rats at 5, 24, and 48 hr. Sepsis was induced by injecting live Escherichia coli bacteria intraperitoneally. Sepsis attenuated the fasting-induced increase in beta-hydroxybutyrate and reduced liver and serum triglycerides at 5 hr. There was a percentage decline in the most abundant fatty acids in neutral lipids, namely oleic (18:1w9) and linoleic (18:2w6) acids. This was seen throughout fasting and septic fasting. These results indicate that 18:1w9 and 18:2w6 are used as energy substrates and are oxidized to beta-hydroxybutyrate during fasting and mainly to carbon dioxide during septic fasting. On the contrary, the most abundant fatty acids in phospholipids, stearic (18:0), arachidonic (20:4w6), and docosahexaenoic (22:6w3) acids, accumulated in neutral lipids and in phospholipids throughout fasting. However, during sepsis this accumulation was reduced in neutral lipids and reversed to a level below that in the fed and fasted state in phospholipids. These results indicate that a disturbance in membrane integrity and function induced by septic fasting may have pathophysiological consequences for lipid metabolism and liver function during sepsis.
研究了禁食和脓毒症期间脂质代谢以及肝脏脂质脂肪酸谱的序贯变化。在正常进食的大鼠以及非脓毒症和脓毒症禁食大鼠的5小时、24小时和48小时采集肝脏和血液样本。通过腹腔注射活的大肠杆菌诱导脓毒症。脓毒症减弱了禁食诱导的β-羟基丁酸增加,并在5小时时降低了肝脏和血清甘油三酯水平。中性脂质中最丰富的脂肪酸,即油酸(18:1w9)和亚油酸(18:2w6)的含量百分比下降。在整个禁食和脓毒症禁食期间均观察到这种情况。这些结果表明,18:1w9和18:2w6在禁食期间用作能量底物并被氧化为β-羟基丁酸,而在脓毒症禁食期间主要被氧化为二氧化碳。相反,磷脂中最丰富的脂肪酸,即硬脂酸(18:0)、花生四烯酸(20:4w6)和二十二碳六烯酸(22:6w3),在整个禁食期间在中性脂质和磷脂中均有积累。然而,在脓毒症期间,这种积累在中性脂质中减少,在磷脂中则逆转至低于进食和禁食状态的水平。这些结果表明,脓毒症禁食引起的膜完整性和功能紊乱可能对脓毒症期间的脂质代谢和肝功能产生病理生理后果。