 再累再忙也要注意身体 新的一周 代谢学人陪您一起品荐读 1、线粒体蛋白Opa1通过尿素循环代谢物促进脂肪细胞棕色化 中文摘要 拓展阅读 尿素循环（UC） UC循环在肝脏中存在是公认的。然而也有报道除肝脏外，脂肪中也存在参与UC循环的酶。2015年的一篇文献中作者证实大鼠的SAT中有一整套UC循环的酶。然而作者的研究结论是脂肪组织中并不进行完整的UC循环，而是提供参与UC循环的中间产物，补充肝脏的UC循环。目前对于脂肪与UC循环的研究，一般认为脂肪组织参与精氨酸和瓜氨酸代谢，而这两种氨基酸代谢与UC循环密切相关。因此脂肪组织的代谢状态（主要是氨基酸代谢）也能够影响UC循环。 UC循环和TCA循环的联系：精氨酸代琥珀酸在ASL的作用下生成延胡索酸和精氨酸，UC循环中产生的延胡索酸进入TCA循环，而TCA循环产生的草酰乙酸转变为天冬氨酸进入UC循环。UC循环与TCA循环的联系是基于精氨酸代琥珀酸的断裂与形成实现的。 参考文献： [1] Bigot A, et al. J Inherit Metab Dis. 2017Nov;40(6):757-769. [2] Keshet R, et al. Nat Rev Cancer. 2018 Oct;18(10):634-645. [3] Sofiía Arriarán, et al. RSC Advances. 2015 Oct; 5，93403-93414. The mitochondrial protein Opa1 promotes adipocyte browning that is dependent on urea cycle metabolites. 一作：Bean, C., Audano,M., Varanita, T.，PI：Nico Mitro, LucaScorrano 发表单位：Department of Biology,University of Padova Abstract 原文链接：https://www./articles/s42255-021-00497-2
2、过氧化物酶体β-氧化作为胞内脂肪酸传感器调节脂解 中文摘要 拓展阅读 过氧化物酶体的β-氧化 参考文献： [1] Wanders, R. J. A. Biochimie 98, 36–44 (2014). [2]Boveris, A., Oshino, N. & Chance, B. Biochem. J. 128,617–630 (1972). Peroxisomal β-oxidation acts as a sensor for intracellular fatty acids and regulates lipolysis 一作：Lianggong Ding，PI：Markus Heim ,ChristianWolfrum 发表单位：Institute of Food,Nutrition and Health Abstract To liberate fatty acids (FAs) from intracellular stores,lipolysis is regulated by the activity of the lipases adipose triglyceridelipase (ATGL), hormone-sensitive lipase and monoacylglycerol lipase. ExcessiveFA release as a result of uncontrolled lipolysis results in lipotoxicity, whichcan in turn promote the progression of metabolic disorders. However, whethercells can directly sense FAs to maintain cellular lipid homeostasis is unknown.Here we report a sensing mechanism for cellular FAs basedon peroxisomal degradation of FAs and coupled with reactive oxygen species(ROS) production, which in turn regulates FA release by modulatinglipolysis. Changes in ROS levels are sensed by PEX2, which modulates ATGLlevels through post-translational ubiquitination. We demonstrate the importanceof this pathway for non-alcoholic fatty liver disease progression using geneticand pharmacological approaches to alter ROS levels in vivo, whichcan be utilized to increase hepatic ATGL levels and ameliorate hepaticsteatosis. The discovery of this peroxisomal β-oxidation-mediated feedbackmechanism, which is conserved in multiple organs, couples the functions ofperoxisomes and lipid droplets and might serve as a new way to manipulatelipolysis to treat metabolic disorders. 原文链接：https://pubmed.ncbi.nlm./34903883/
3、微生物代谢物δ-甜菜碱是一种依赖饮食的肥胖素 肥胖和肥胖相关的代谢紊乱与肠道微生物群有关。然而，微生物群落-宿主相互作用影响能量代谢的因果关系仍存在争议。本文中，科研人员发现微生物组衍生的代谢物 δ-甜菜碱 (VB) 是一种依赖饮食的肥胖素，它会随着肥胖表型的出现而增加，并且与人类的内脏脂肪重量正相关。VB 在无菌小鼠及其线粒体中不存在，但当将无菌小鼠有菌环境适应、发展出肠道菌群后，发现在这些有菌小鼠及其线粒体中存在VB。体内体外机制研究表明，VB 由多种细菌产生，并通过降低胞内肉碱和线粒体长链酰基辅酶A水平来抑制线粒体脂肪酸氧化。对无菌小鼠和常规小鼠给药VB，发现VB会增加内脏脂肪质量并加剧西方饮食下的肝脏脂肪变性，但在普通饮食下未观察到这一现象。因此，VB提供了一个分子靶标来了解饮食依赖型肥胖症中的微生物组-宿主的共生关系或共生失调，从而提供了潜在的干预手段。拓展阅读 微生物组和宿主线粒体之间的关联
参考文献： [1]Bajpai P,etal. Mitochondrion. 2018;39:20-25. [2]Yardeni T, et al. Sci Signal. 2019;12(588):eaaw3159. Microbialmetabolite delta-valerobetaine is a diet-dependent obesogen一作：Ken H.Liu, Joshua A. Owens, Bejan Saeedi，PI：AndrewS. Neish, Dean P. Jones 发表单位：Divisionof Pulmonary, Allergy, Critical Care and Sleep Medicine, Department of Medicine Abstract Obesity and obesity-related metabolic disorders are linked to the intestinal microbiome. However, the causality of changes in the microbiome–host interaction affecting energy metabolism remains controversial. Here, we show the microbiome-derived metabolite δ-valerobetaine (VB) is a diet-dependent obesogen that is increased with phenotypic obesity and is correlated with visceral adipose tissue mass in humans. VB is absent in germ-free mice and their mitochondria but present in ex-germ-free conventionalized mice and their mitochondria. Mechanistic studies in vivo and in vitro show VB is producedby diverse bacte- rial species and inhibits mitochondrial fatty acid oxidation through decreasing cellular carnitine and mitochondrial long-chainacyl-coenzyme As. VB administration to germ-free and conventional mice increases visceral fat mass and exacerbates hepatic steatosis with a westerndiet but not control diet. Thus, VB provides a molecular target to understandand potentially manage microbiome–host symbiosis or dysbiosis in diet-dependent obesity. 原文链接：https://www./articles/s42255-021-00502-8
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