著者

寺本 民生 木下 誠 桂川 敬太 岡崎 聡子 山中 正己 永好 昭 大濱 知子 松木 則夫 斎藤 洋

出版者

一般社団法人 日本動脈硬化学会

雑誌

動脈硬化 (ISSN:03862682)

巻号頁・発行日

vol.22, no.6-7, pp.465-470, 1994-10-25 (Released:2011-09-21)

参考文献数

6

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We found that fatty liver is easily induced in a novel experimental animal, Suncus murinus (suncus) by withholding food. Hepatic triglyceride content increased linearly for up to 24 hours after fasting in these animals, while the glycogen content decreased. Although the glycogen contents returned to the level before fasting at 12 hours after refeeding, the triglyceride contents decreased gradually but did not reach to the level before fasting even at 24 hours after refeeding in suncus. Plasma lipids, glucose and insulin levels decreased by fasting and returned to the levels before fasting between 8 and 24 hours after refeeding. On the other hand, the plasma levels of free fatty acid and ketone bodies were elevated significantly by fasting and decreased rapidly by refeeding. These responses to fasting and refeeding except for the change in hepatic triglyceride are in common with other experimental animals, suggesting that there are no abnormalities not only in glucose metabolism but also in fatty acid metabolism.The study of lipoproteins from this animal revealed that small amounts of lipoproteins with apolipoprotein (apo) E but without apoB were observed in the fraction of density less than 1.08g/ml. In order to learn whether apoB is synthesized by the liver or not, isolated suncus livers were perfused with an addition of [35S] methionine. Small amounts of radioactivity were observed in apoE of VLDL, and fairly large amounts in apoE and A-I in the fraction of LDL+HDL, suggesting that VLDL was secreted with apoE but not with apoB from the liver. Northern blot analysis with use of rat apoB cDNA revealed a weak signal of hybridized rat apoB cDNA between 15Kb and 9Kb in the suncus liver and intestinal mucosa; this is almost the same size as rat apoB mRNA. This finding suggests the presence of apoB mRNA in the suncus.In conclusion, apoB is not secreted from the suncus liver, owing to a defect in intracellular posttranscriptional processing or to ineffective transcription. This might be one of the reasons for fatty deposits in the suncus liver. Suncus may be a candidate for an animal model of abetalipoproteinemia as well as fatty liver due to a defect of apoB synthesis.