首页> 外文期刊>Comparative biochemistry and physiology. Toxicology & pharmacology: CBP >SUPPLEMENTATION OF COCONUT OIL FROM DIFFERENT SOURCES TO THE DIET INDUCES CELLULAR DAMAGE AND RAPID CHANGES IN FATTY ACID COMPOSITION OF CHICK LIVER AND HEPATIC MITOCHONDRIA
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SUPPLEMENTATION OF COCONUT OIL FROM DIFFERENT SOURCES TO THE DIET INDUCES CELLULAR DAMAGE AND RAPID CHANGES IN FATTY ACID COMPOSITION OF CHICK LIVER AND HEPATIC MITOCHONDRIA

机译:补充椰子油到饮食中会引起鸡肝和肝线粒体脂肪酸组成的细胞损伤和快速变化

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Supplementation of 20% coconut oil from two commercial sources, pharmaceutical (''Pharmacy'') and cooking (''Pastry'') use, to the chick diet for 14 days produced a clear damage to the hepatic mitochondria, accompanied by an accumulation of glycogen and lipid droplets in the hepatocyte cytoplasm. These effects may be accounted for the high proportion of fat supplemented to the diets (20%). Pharmacy coconut oil induced a high percentage of cellular death when administered for 14 days. Fatty acid profiles in liver and hepatic mitochondria rapidly changed (24 hr) after both coconut oils supplementation to the diet. The accumulation of shorter chain fatty acids (12:0 and 14:0) was always higher after Pharmacy than after Pastry diet feeding. This fact may contribute, at least in part, to the cellular damage mentioned above especially after Pharmacy diet feeding. Mitochondrial ratios of saturated/unsaturated and saturated/polyunsaturated fatty acids rapidly changed in parallel to these ratios in both diets. Most of the mitochondrial parameters measured tend to recuperate the control Values when diets were supplied for 5-14 days. Nevertheless, the maintenance of the mentioned ratios after 14-days Pharmacy diet feeding at significantly higher levels than those observed in control, seems to suggest the lack of the homeostatic mechanism in these membranes and could be also related with the high percentage of cellular death observed after this dietary manipulation. (C) 1997 Elsevier Science Inc. [References: 26]
机译:从雏鸡的饮食中补充两种商业来源的20%椰子油(制药(“ Pharmacy”)和烹饪(“ Pastry”))对鸡的饮食产生了明显的肝线粒体损害,并伴有堆积肝细胞质中糖原和脂滴的变化这些影响可能是饮食中补充脂肪的比例很高(20%)。服用14天后,药房椰子油会引起很高的细胞死亡百分比。两种椰子油补充饮食后,肝脏和肝线粒体中的脂肪酸谱快速变化(24小时)。药房后,短链脂肪酸(12:0和14:0)的积累始终高于糕点饮食喂养后。这个事实可能至少部分是造成上述细胞损伤的原因,尤其是在药房饮食喂养之后。在两种饮食中,饱和/不饱和脂肪酸和饱和/多不饱和脂肪酸的线粒体比率均与这些比率平行快速变化。当提供日粮5-14天时,测得的大多数线粒体参数趋于恢复对照值。然而,在14天药房饮食喂养后,上述比例的维持水平显着高于对照中观察到的水平,似乎表明这些膜缺乏稳态机制,也可能与观察到的高细胞死亡百分比有关经过这种饮食控制。 (C)1997 Elsevier Science Inc. [参考:26]

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