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[蛋白质营养不良时的肝脏变化。大鼠实验研究]

[Liver changes in protein malnutrition. An experimental study in rats].

作者信息

Conde Martel A, González Reimers E, Santolaria Fernández F, Castro Alemán V, Marchena Gómez J, Martínez Riera A

机构信息

Servicio de Medicina Interna, Hospital Universitario de Canarias, España.

出版信息

Nutr Hosp. 1993 Jul-Aug;8(6):358-63.

PMID:8373879
Abstract

It is known that protein malnutrition conditions the development of liver steatosis, and may be accompanied by fibrosis. Ito cells intervene in the fibrogenesis, converting to transitional cells and myofibroblasts. Some trace elements, such as copper (Cu), iron (Fe) and manganese (Mn) act as co-factors, and zinc (Zn) acts as an inhibitor of a variety of enzymes involved in the collagen synthesis. This study analyzes the effects on the livers of 12 mate Wistar rats following two months administration of a hypoproteic (6%) isocaloric diet, comparing histomorphometric parameters (hepatocyte and nucleum area, total fat and fibrosis) and the liver content in Fe, Cu, Zn and Mn, with those in 12 control rats of similar age and sex. The experimental group revealed a significant reduction in hepatocyte nucleum area (p < 0.001), an increase in the ratio of hepatocyte cytoplasmatic and nucleum hepatocyte area, pronounced steatosis and slight fibrosis. No differences were found in Ito cell percentages. The experimental group showed a significant increase in liver content of Fe (p = 0.01) and a significant drop in Mn content (p < 0.01), Zn (p = 0.05) and Cu (p < 0.01). Liver iron content correlated significantly with total fat level (p = 0.03).

摘要

众所周知,蛋白质营养不良会引发肝脂肪变性,并且可能伴有纤维化。肝星状细胞参与纤维化形成过程,会转变为过渡细胞和成肌纤维细胞。一些微量元素,如铜(Cu)、铁(Fe)和锰(Mn)作为辅因子起作用,而锌(Zn)则作为参与胶原蛋白合成的多种酶的抑制剂。本研究分析了对12只雄性Wistar大鼠连续两个月给予低蛋白(6%)等热量饮食后肝脏的影响,将组织形态计量学参数(肝细胞和细胞核面积、总脂肪和纤维化)以及肝脏中Fe、Cu、Zn和Mn的含量与12只年龄和性别相似的对照大鼠进行比较。实验组肝细胞细胞核面积显著减小(p < 0.001),肝细胞细胞质与细胞核面积之比增加,出现明显的脂肪变性和轻微纤维化。肝星状细胞百分比未发现差异。实验组肝脏中Fe含量显著增加(p = 0.01),Mn含量显著下降(p < 0.01),Zn(p = 0.05)和Cu(p < 0.01)。肝脏铁含量与总脂肪水平显著相关(p = 0.03)。

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