Obesity and steatosis promotes mitochondrial remodeling that enhances respiratory capacity in the liver of ob/ob mice
Obesity and steatosis promotes mitochondrial remodeling that enhances respiratory capacity in the liver of ob/ob mice
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DOI：
10.1002/1873-3468.13005
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发表时间：
2018-03-01
期刊：
影响因子：
3.5
通讯作者：
Han, Derick
中科院分区：
文献类型：
--
作者：
Garcia, Jerome;Decker, Carl W.;Han, Derick
我们研究了肥胖/脂肪变性是否促进ob/ob小鼠（肥胖模型）肝脏中的线粒体重塑。对于检查的所有呼吸底物（谷氨酸/苹果酸、琥珀酸、辛酸和甘油3-磷酸），与对照组（C57 BL/6 J、C57 BL/6 NJ）相比，ob/ob小鼠（21周，具有显著脂肪变性）的肝线粒体在状态III呼吸中具有相似的2倍增加。在成熟ob/ob小鼠的肝线粒体中，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）的表达相应增加2倍。相反，对于检查的任何呼吸底物，幼年ob/ob小鼠（6周）的肝脏线粒体呼吸与对照组没有差异。总体而言，增强呼吸的线粒体重塑随着ob/ob小鼠肝脏中的肥胖/脂肪变性而增加。
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 similar to 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.