Effect of dietary fat on Ito cell activation by chronic ethanol intake: a long-term serial morphometric study on alcohol-fed and control rats.
Effect of dietary fat on Ito cell activation by chronic ethanol intake: a long-term serial morphometric study on alcohol-fed and control rats.
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膳食脂肪对慢性乙醇摄入对 Ito 细胞活化的影响：对酒精喂养和对照大鼠的长期系列形态测量研究。
DOI：
10.1111/j.1530-0277.1991.tb05212.x
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
French,SW
中科院分区：
文献类型：
--
作者：
Takahashi,H;Wong,K;Jui,L;Nanji,AA;Mendenhall,CS;French,SW
我们研究了长期乙醇摄入和膳食脂肪对大鼠Ito细胞活化的影响。将16对Wistar雄性大鼠分为两组，一组饲喂牛脂，另一组饲喂玉米油作为膳食脂肪来源。每组大鼠成对喂食营养充足的流质饲料，其中含有玉米油（CF）或牛脂（TF）作为脂肪以及蛋白质和碳水化合物。每组中的一半接受乙醇，其余的通过植入的胃管成对喂食等热量的右旋糖，长达5个月。在每月活检（包括基线）的电子显微照片上对Ito细胞的脂肪和粗面内质网（RER）变化进行形态计量分析。通过Ito细胞中脂肪/RER比率的降低来评估Ito细胞活化。在酒精大鼠的Ito细胞的脂肪/粗面内质网的比例喂养CF饮食（CFA）逐渐下降。在喂养5个月时，发现该比率低于配对喂养的对照大鼠（CFC）。CFA分别为1.74 ± 0.57和7.46 ± 2.05，p <0.05，均数± se）。Ito细胞脂肪在5个月时也显著降低（p <0.05）。CFA中的脂肪/粗面内质网比值仅在脂肪变化、坏死和炎症发生后显著降低，随后发生肝纤维化。相反，TFA大鼠在整个研究期间Ito细胞中的脂肪/RER比率没有显着降低，而TFC大鼠的脂肪/RER比率则有所增加。在CFC、TFA和TFC大鼠的肝脏中观察到极轻微的病理变化。这些结果表明，Ito细胞的激活在一个显着的水平只发生在后期的过程中，中度至重度异常的肝脏组织学已经发展，虽然激活可能已经开始在乙醇喂养的早期。结果表明，膳食脂肪酸组成可能是乙醇诱导的Ito cII激活的发病机制中的一个重要因素。
We studied the effects of long‐term ethanol ingestion and dietary fat on Ito cell activation morphometrically in rats. Sixteen pairs of Wistar male rats were divided into two groups, one fed tallow and the other fed corn oil as the source of dietary fat. Each group of rats were pair‐fed a nutritional adequate liquid diet containing either corn oil (CF) or tallow (TF) as fat as well as protein and carbohydrate. Half of each group received ethanol, the rest were pair‐fed isocaloric amounts of dextrore via an implanted gastric tube for up to 5 months. Morphometric analysis of the change in fat and rough endoplasmic reticulum (RER) of Ito cells was performed on electron micrographs obtained from monthly biopsies including baseline. Ito cell activation was assessed by a decrease in the ratio of fat/RER in Ito cells. The ratio of fat/RER in Ito cells of alcoholic rats fed the CF diet (CFA) gradually decreased. The ratio war found to be lower than in the pair‐fed control rats (CFC) at 5 months of feeding. CFA 1.74 ± 0.57, vs. 7.46 ± 2.05, respectlvely, p < 0.05, mean ± se). Ito cell fat also significantly decreased at 5 months of feeding (p < 0.05). The fat/ RER ratio In CFA significantly decreased only subsequent to the development of fatty change, necrosis, and inflammation followed by fibrosis of the liver. In contrast, the TFA rats did not show a significant decrease in the fat/RER ratio in the Ito cells throughout the study, while TFC rats showed an increase in the fat/RER ratio. Minimal pathological changes were observed In the livers of CFC, TFA, and TFC rats. These results indicate that activation of Ito cells at a signifiant level occurred only late in the course of feeding alcohol after moderate to severe abnormalities in liver hlstology had developed, although activation may have begun at an earlier time of ethanol feeding. The results Indicate that dietary fatty acid composition may be an important factor in the pathogenesis of ethanol‐induced Ito cII activation.
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