Ohama T, Matsuki N, Saito H, Tsukamoto K, Kinoshita M, Katsuragawa K, Okazaki S, Yamanaka M, Teramoto T
Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, University of Tokyo.
J Biochem. 1994 Feb;115(2):190-3. doi: 10.1093/oxfordjournals.jbchem.a124316.
We have previously reported that fatty liver is easily induced in a novel experimental animal, Suncus murinus (suncus) by withholding food, and that apolipoprotein B (apo B) is not actively synthesized in the liver. In the present paper we describe the effect of starving and refeeding on lipid and lipoprotein metabolism in suncus, in order to explore the mechanisms of induction of fatty liver by starving and of its improvement by refeeding. Starvation induced increase in triglyceride content and decrease in glycogen content of the liver. Although the glycogen content returned to the level before starvation at 12 h after refeeding, the triglyceride content decreased gradually but did not reach the prestarvation level even at 24 h after refeeding in suncus. Plasma lipids, glucose, and insulin levels were decreased by starvation and returned to the levels before starvation between 8 and 24 h after refeeding. On the other hand, the plasma levels of free fatty acid and ketone bodies were elevated significantly by starvation and decreased rapidly by refeeding. These responses to starvation and refeeding, except for the change in hepatic triglyceride, are in common with other experimental animals, suggesting that there are no abnormalities in glucose metabolism or in fatty acid metabolism in suncus. In conclusion, the fatty liver induced by starvation in suncus may be caused by impaired triglyceride transport out of the liver, for which apolipoprotein B is mostly responsible, as reported previously.
我们之前报道过，通过禁食可在一种新型实验动物——臭鼩鼱（suncus）中轻易诱导出脂肪肝，并且肝脏中载脂蛋白B（apo B）并非活跃合成。在本文中，我们描述了禁食和再喂食对臭鼩鼱脂质和脂蛋白代谢的影响，以探究禁食诱导脂肪肝及其通过再喂食改善的机制。禁食导致肝脏甘油三酯含量增加，糖原含量减少。尽管再喂食12小时后糖原含量恢复到禁食前水平，但臭鼩鼱再喂食24小时后甘油三酯含量仍逐渐下降，甚至未达到禁食前水平。禁食使血浆脂质、葡萄糖和胰岛素水平降低，再喂食8至24小时后恢复到禁食前水平。另一方面，禁食显著提高了血浆游离脂肪酸和酮体水平，再喂食后迅速下降。除肝脏甘油三酯变化外，这些对禁食和再喂食的反应与其他实验动物相同，表明臭鼩鼱的糖代谢或脂肪酸代谢无异常。总之，如之前报道的那样，臭鼩鼱禁食诱导的脂肪肝可能是由于肝脏甘油三酯转运受损所致，而这主要由载脂蛋白B负责。
