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成年大鼠棕色脂肪组织中禁食诱导的线粒体蛋白质降解的饮食调节

Dietary regulation of fasting-induced mitochondrial protein degradation in adult rat brown adipose tissue.

作者信息

Puigserver P, Palou A, Gianotti M

机构信息

Departament de Biologia Fonamental i Ciències de la Salut, Institut d'Estudis Avançats-Universitat de les Illes Balears, Palma de Mallorca, Spain.

出版信息

Biochem Int. 1992 Sep;27(6):1037-46.

PMID:1332718
Abstract

Mitochondrial protein, cytochrome-c-oxidase and mitochondrial ATPase activities, which can participate in brown adipose tissue thermogenesis, were measured in the present study in order to evaluate mitochondrial activity, oxidative capacity and ATP synthesis in dietary obese rats compared to control rats. Cafeteria-diet induced increase of cytochrome-c-oxidase and ATPase activities of 54% and 37% respectively, but mitochondrial protein content remained unchanged. Fasting induced active mitochondrial protein degradation (about 50%) only in control rats, but in both cafeteria fed and post-cafeteria obese rats fasting-induced loss of mitochondrial protein was impaired. It was concluded that cafeteria diet is able to induce specifically both the oxidative capacity and the ATP synthesis in adult rat brown adipose tissue without affecting the mitochondrial protein. Furthermore, during fasting the obese (or overweight) status 'per se' regulates the overall mitochondrial protein degradation which was impaired or inactivated in overweight dietary rats compared with controls.

摘要

本研究测定了可参与棕色脂肪组织产热的线粒体蛋白、细胞色素 c 氧化酶和线粒体 ATP 酶活性,以评估饮食诱导肥胖大鼠与对照大鼠相比的线粒体活性、氧化能力和 ATP 合成。自助餐式饮食分别使细胞色素 c 氧化酶和 ATP 酶活性增加了 54%和 37%,但线粒体蛋白含量保持不变。禁食仅在对照大鼠中诱导了活跃的线粒体蛋白降解(约 50%),但在自助餐喂养和自助餐喂养后的肥胖大鼠中,禁食诱导的线粒体蛋白损失均受到损害。得出的结论是,自助餐式饮食能够特异性地诱导成年大鼠棕色脂肪组织的氧化能力和 ATP 合成,而不影响线粒体蛋白。此外,在禁食期间,肥胖(或超重)状态本身调节总体线粒体蛋白降解,与对照组相比,超重饮食大鼠的这种降解受到损害或失活。

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