Cell Metabolism十周年特刊：新陈代谢十大突破

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Cell metabolism创刊十周年之际，主编盘点了以下十大的突破:
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% g/ i6 R$ O" ?  G; W7 I1.系统生物学6 F: H2 C# a6 z

* k* b9 i% R0 K9 K. I8 l( k6 gSystems-based approaches tackle the complex interplay of genetic, molecular, and environmental factors contributing to metabolic diseases by integrating a range of “omics” data.
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0 Z' G9 [0 E( k系统生物学通过整合各种“组学”来研究基因，分子和环境层面的各种相互作用对代谢类疾病的影响。3 V. S$ @5 \. y+ l) W; O; Y
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2.PSCK9和LDL-R降解
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& o7 E  Y/ _. qPCSK9 targets LDL-R for degradation and raises plasma LDL cholesterol. Anti-PCSK9 therapies, currently in clinical trials, represent a promising new treatment for hypercholesterolemia.
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PCSK9靶向低密度胆固醇受体（LDL-R)，提高血液中低密度胆固醇（LDL)的水平。目前针对PCSK9的治疗策略，正在进入临床测试阶段，可能为治疗高胆固醇血症开辟新的途径。) u/ J! q& G6 O9 Q5 x
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3.新陈代谢的总控制
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$ [% {3 \4 f4 \; Y' ], ]; J( XLeptin and other hormones control body weight via a neuronal network, rather than a single set of cells. The brain also directly regulates glucose metabolism.4 V. [7 |: _. h! w' A
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瘦素和其他激素通过复杂的神经网络而不是某种细胞群来调控我们的体重，大脑直接控制着葡萄糖的代谢。0 g2 G) D* U4 v; E+ @: X
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4.选择性地胰岛素耐受3 k, Y% _! _3 k
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Distinct tissues/cells resist differently to the anabolic effects of insulin, a phenomenon first recognized in the liver, where insulin promoted lipogenesis without suppressing glucose production.
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不同的组织和细胞选择性的抵抗胰岛素促合成代谢的效果。最先在肝脏中发现了胰岛素抵抗，胰岛素本应该被肝脏吸收促进糖原的合成，降低血糖，胰岛素抵抗却促进了脂肪的生成。
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5.FGF家族和新陈代谢
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FGFs, including FGF1, 15/19, 21, and 23, emerged as key metabolic regulators, and an FGF21 mimetic showed therapeutic promise in obese diabetic humans.3 E/ h4 i, s# U2 B! h9 e8 E

9 X. A+ [1 Q2 e: _2 ]FGF生长因子家族包括FGF1，15/19，21，23，被证明具有调控代谢的作用。类FGF21的分子更是在肥胖型糖尿病患者身上显示出治疗效果。
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: a  w' m( P! G; f2 [1 g- w, r' \6.人体内的棕脂肪
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$ Y  R5 N) s: @1 G1 X2 j/ w1 iInitially thought to be restricted to infants, small rodents, and hibernating animals, metabolically active BAT was also found in adult humans in 2009.( f  s1 Z: k2 s: {" c2 i+ E

; \8 q: D  ~5 X& e. w原本以为棕脂肪只存在于婴儿，鼠类和冬眠动物中，2009年的一篇论文发现成人体内也存在着积极参与代谢的棕脂肪。
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7.癌症的代谢! Z# I+ b' n+ Q
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Cancer cells rewire their metabolism in unique ways, such as aerobic glycolysis, also known as the “Warburg effect,” and reductive carboxylation, to rapidly proliferate and survive.4 T7 ]8 m4 N/ H- Z0 A& [2 [8 D* Z
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癌细胞有着特有的代谢方式包括无氧糖酵解，也被称为“Warburg效应”，以及还原性羧化作用来快速增殖和存活。9 C8 `- _/ G7 F0 k* C
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8.肠道微生物组
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- f! q  t1 \7 g1 X5 Z" v1 U! n/ uThe gut contains trillions of microbes that can shape the host’s metabolism and immune system and contribute to obesity and the metabolic syndrome.
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人的肠道中有着数万亿的细菌，它们可以影响我们的代谢和免疫系统，关系到我们的肥胖和代谢综合征。
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, O! Y- G3 D2 A; ?9.表观遗传影响新陈代谢1 ~; F4 `" i% I( F+ h5 s% H

, l6 p6 [5 e. ~# c9 ?/ ~Chromatin modifications in response to extracellular cues, including during early life, regulate metabolic gene expression and may contribute to metabolic disease susceptibility.( W( ]' G" |" \/ h: l/ |. u

, I2 p9 v# B4 i/ Z7 e2 D- a4 N1 v4 A包括新生时期在内的胞外信号会影响染色体的修饰，从而调控和代谢相关的基因表达，进而影响到我们代谢综合征的易感性。
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4 p% V* Y4 m* S  P. v9 B) _- T7 u  j10.免疫新陈代谢
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) m  L% m* k* Q, Y: B; P$ ]6 LObesity and inflammation are recognized to go hand in hand, and several immune cells (macrophages, NK, T, and B cells) are found to influence metabolic disease pathogenesis.0 \' C2 R2 i! j
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肥胖和炎症如影随形。免疫细胞（包括巨噬细胞，自然杀伤细胞，T细胞，B细胞）都参与了代谢类疾病的发病过程。(转载自生物谷)$ c( e3 `5 P+ l8 }  u, p+ A; ^
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英文原文报道：10 YEARS of Cell Metabolism.
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