Suppr超能文献

高脂饮食对大鼠肝脏线粒体中超氧阴离子生成及膜流动性的影响。

Effects of a high-fat diet on superoxide anion generation and membrane fluidity in liver mitochondria in rats.

作者信息

Togo M, Konari N, Tsukamoto M, Kimoto R, Yamaguchi T, Takeda H, Kambayashi I

机构信息

1Graduate School of Dairy Sciences, Rakuno Gakuen University, 582, Midorimachi Bunkyodai, Ebetsu, Hokkaido 069-8501 Japan.

2Graduate School of Medicine, Sapporo Medical University, S1 W17, Chuo-ku, Sapporo, Hokkaido 060-8556 Japan.

出版信息

J Int Soc Sports Nutr. 2018 Mar 14;15:13. doi: 10.1186/s12970-018-0217-z. eCollection 2018.

Abstract

BACKGROUND

Obesity is a primary factor of lifestyle-related diseases, and the age of its onset has decreased. The reactive oxygen species (ROS), the superoxide anion, is generated in the mitochondrial electron transport chain and the damage it induces in cells may be a contributing factor to obesity-related lifestyle diseases. In the present study, the influence of the ingestion of a high-fat diet (HFD) on superoxide anion generation in rat liver mitochondria (Mt) and membrane fluidity was investigated.

METHODS

Male Wistar rats were fed a normal diet (ND,  = 6) or HFD ( = 6). Liver Mt were isolated and oxygen consumption, superoxide anion production (the adrenaline method), and membrane fluidity (the spin label method) were measured.

RESULTS

After 11 weeks, body weights and abdominal circumferences were higher in the HFD group than in the ND group. Mt oxygen consumption was higher in the HFD group than in the ND group. Superoxide anion production was significantly lower in the HFD group than in the ND group, while no significant changes were observed in membrane fluidity.

CONCLUSION

Although rats developed diet-induced obesity, it did not reach the level of disease development. The promotion of lipid metabolism appeared to reduce superoxide anion production, but did not influence membrane fluidity. While superoxide anion damages cells as an oxidative stress, ROS and superoxide dismutase are essential signaling molecules in the body. The present results suggest that the continuous ingestion of a HFD impairs Mt and induces disease development.

摘要

背景

肥胖是与生活方式相关疾病的主要因素,且其发病年龄已降低。活性氧(ROS),即超氧阴离子,在线粒体电子传递链中产生,其对细胞造成的损伤可能是肥胖相关生活方式疾病的一个促成因素。在本研究中,研究了高脂饮食(HFD)摄入对大鼠肝脏线粒体(Mt)中超氧阴离子生成及膜流动性的影响。

方法

将雄性Wistar大鼠分为正常饮食组(ND,n = 6)或高脂饮食组(n = 6)。分离肝脏Mt并测量氧气消耗、超氧阴离子产生(肾上腺素法)和膜流动性(自旋标记法)。

结果

11周后,高脂饮食组的体重和腹围高于正常饮食组。高脂饮食组的Mt氧气消耗高于正常饮食组。高脂饮食组的超氧阴离子产生显著低于正常饮食组,而膜流动性未观察到显著变化。

结论

尽管大鼠出现了饮食诱导的肥胖,但未达到疾病发展水平。脂质代谢的促进似乎减少了超氧阴离子的产生,但未影响膜流动性。虽然超氧阴离子作为氧化应激会损伤细胞,但ROS和超氧化物歧化酶是体内重要的信号分子。目前的结果表明,持续摄入高脂饮食会损害Mt并诱导疾病发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07c9/5853147/0baebd4c0dc7/12970_2018_217_Fig1_HTML.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验