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Adipose Fatty Acid Oxidation Is Required for Thermogenesis and Potentiates Oxidative Stress-Induced Inflammation

机译:脂肪脂肪酸氧化是产热所必需的,并能增强氧化应激诱导的炎症

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To understand the contribution of adipose tissue fatty acid oxidation to whole-body metabolism, we generated mice with an adipose-specific knockout of carnitine palmitoyltransferase 2 (CPT2^A^-^/^-), an obligate step in mitochondrial long-chain fatty acid oxidation. CPT2^A^-^/^- mice became hypothermic after an acute cold challenge, and CPT2^A^-^/^- brown adipose tissue (BAT) failed to upregulate thermogenic genes in response to agonist-induced stimulation. The adipose-specific loss of CPT2 resulted in diet-dependent changes in adiposity but did not result in changes in body weight on low- or high-fat diets. Additionally, CPT2^A^-^/^- mice had suppressed high-fat diet-induced oxidative stress and inflammation in visceral white adipose tissue (WAT); however, high-fat diet-induced glucose intolerance was not improved. These data show that fatty acid oxidation is required for cold-induced thermogenesis in BAT and high-fat diet-induced oxidative stress and inflammation in WAT.
机译:为了了解脂肪组织脂肪酸氧化对全身代谢的贡献,我们制备了具有脂肪特异性敲除肉碱棕榈酰转移酶2(CPT2 ^ A ^-^ / ^-)的小鼠,这是线粒体长链脂肪中的专一步骤酸氧化。在急性冷攻击后,CPT2 ^ A ^-^ / ^-小鼠变为低温,并且CPT2 ^ A ^-^ / ^-棕色脂肪组织(BAT)不能响应激动剂诱导的刺激而上调产热基因。 CPT2的特定于脂肪的损失导致了肥胖的饮食依赖性变化,但在低脂或高脂饮食中并未导致体重变化。另外,CPT2 ^ A ^-^ / ^-小鼠抑制了高脂饮食诱导的内脏白色脂肪组织(WAT)的氧化应激和炎症。然而,高脂饮食诱导的葡萄糖耐量没有改善。这些数据表明,脂肪酸氧化是BAT中冷诱导的热生成和WAT中高脂饮食诱导的氧化应激和炎症所必需的。

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