脂肪组织脂肪酸氧化是产热所必需的，并增强氧化应激诱导的炎症反应。
Adipose fatty acid oxidation is required for thermogenesis and potentiates oxidative stress-induced inflammation.
作者信息
Lee Jieun, Ellis Jessica M, Wolfgang Michael J
机构信息
Department of Biological Chemistry, Center for Metabolism and Obesity Research, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Department of Biological Chemistry, Center for Metabolism and Obesity Research, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
出版信息
Cell Rep. 2015 Jan 13;10(2):266-79. doi: 10.1016/j.celrep.2014.12.023. Epub 2015 Jan 8.
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.
为了解脂肪组织脂肪酸氧化对全身代谢的贡献，我们构建了肉碱棕榈酰转移酶2（CPT2(A-/-)）脂肪特异性敲除小鼠，这是线粒体长链脂肪酸氧化的一个必要步骤。CPT2(A-/-)小鼠在急性冷刺激后体温降低，且CPT2(A-/-)棕色脂肪组织（BAT）在激动剂诱导刺激下未能上调产热基因。CPT2的脂肪特异性缺失导致肥胖的饮食依赖性变化，但在低脂或高脂饮食下体重并未改变。此外，CPT2(A-/-)小鼠在内脏白色脂肪组织（WAT）中抑制了高脂饮食诱导的氧化应激和炎症；然而，高脂饮食诱导的葡萄糖不耐受并未改善。这些数据表明，脂肪酸氧化是BAT冷诱导产热以及WAT高脂饮食诱导的氧化应激和炎症所必需的。
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