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肥胖和脂肪变性促进了线粒体重构,增强了 ob/ob 小鼠肝脏的呼吸能力。

Obesity and steatosis promotes mitochondrial remodeling that enhances respiratory capacity in the liver of ob/ob mice.

机构信息

Department of Biology, University of La Verne, CA, USA.

Department of Biopharmaceutical Sciences, School of Pharmacy, Keck Graduate Institute, Claremont, CA, USA.

出版信息

FEBS Lett. 2018 Mar;592(6):916-927. doi: 10.1002/1873-3468.13005. Epub 2018 Feb 28.

DOI:10.1002/1873-3468.13005
PMID:29430655
Abstract

We investigated if obesity/steatosis promotes mitochondrial remodeling in the liver of ob/ob mice (an obesity model). Liver mitochondria from ob/ob mice (21 weeks with significant steatosis) had ~ 2-fold increases in state III respiration compared with control (C57BL/6J, C57BL/6NJ) for all respiratory substrates examined (glutamate/malate, succinate, octanoate, and glycerol 3-phosphate). A corresponding 2-fold increase in the expression of respiratory complexes (I, IV, and V) and other respiratory proteins (glycerol phosphate dehydrogenase-2 and medium-chain acyl-coenzyme A dehydrogenase) occur in liver mitochondria of mature ob/ob mice. Conversely, respiration in liver mitochondria from young ob/ob mice (6 weeks) does not differ from control with any respiratory substrates examined. Overall, mitochondrial remodeling that enhances respiration increases with obesity/steatosis in the liver of ob/ob mice.

摘要

我们研究了肥胖/脂肪变性是否会促进肥胖症(ob/ob)小鼠肝脏中的线粒体重塑(一种肥胖模型)。与对照(C57BL/6J、C57BL/6NJ)相比,ob/ob 小鼠(21 周龄,有明显的脂肪变性)的肝脏线粒体在所有检测的呼吸底物(谷氨酸/苹果酸、琥珀酸、辛酸盐和甘油 3-磷酸)中,III 态呼吸增加了约 2 倍。成熟 ob/ob 小鼠肝脏线粒体中呼吸复合物(I、IV 和 V)和其他呼吸蛋白(甘油磷酸脱氢酶-2 和中链酰基辅酶 A 脱氢酶)的表达也相应增加了 2 倍。相反,用任何呼吸底物检测,年轻 ob/ob 小鼠(6 周龄)的肝脏线粒体呼吸与对照没有差异。总的来说,随着肥胖症/脂肪变性在 ob/ob 小鼠肝脏中的发展,增强呼吸的线粒体重塑也随之增加。

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