DIABETOLOGIA：去泛素酶USP19可调节小鼠的脂肪生成，增强高脂饮食诱导的肥胖和葡萄糖耐受不良

2019-04-04 不详网络

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对于理解和治疗肥胖这一流行病，阐明脂肪积累的分子机制及其代谢后果使至关重要。我们之前已经观察到。与野生型(WT)小鼠相比，Usp19去泛素酶缺失小鼠(Usp19−/−)的脂肪量显著低。因此，本研究旨在进一步了解泛素特异性肽酶19 (USP19)在脂肪发育、肥胖和糖尿病中的作用。

本研究比较WT和Usp19−/−小鼠的代谢表型。分离WT和Usp19−/−小鼠腹股沟脂肪垫的基质血管组分(SVFs)，培养细胞分化为脂肪细胞，以评估其产脂能力。老鼠被喂食高脂肪食物(HFD) 18周。评估机体组成、葡萄糖代谢和代谢变量。此外，在注射胰岛素后，对肌肉、肝脏和脂肪组织的信号活动进行了分析。最后分析了Usp19 mRNA表达与脂肪组织中脂肪细胞功能基因表达的相关性。

结果显示，与WT小鼠细胞不同，来自Usp19−/−的SVF细胞在脂肪分化时不能积累脂肪并上调脂肪基因。与WT小鼠相比，Usp19−/−小鼠一生中脂肪垫更小，瘦肉比例更高。当喂食HFD时，Usp19−/−小鼠比WT小鼠对葡萄糖、丙酮酸耐受性更强，对胰岛素更敏感。此外，hfc喂养的Usp19−/−小鼠在肌肉和肝脏中增强了胰岛素信号，但在脂肪组织中没有出现类似情况。最后，USP19 mRNA在人脂肪组织中的表达与腹部脂肪库中重要脂肪细胞基因的表达呈正相关，而与皮下脂肪库无关。

研究表明，USP19是脂肪发育的重要调节因子。其在小鼠体内的失活作用对多种组织都有影响，其可能对高脂饲料的负代谢作用有保护作用。这些发现表明，抑制USP19可能具有治疗潜力，以保护免受肥胖和糖尿病的有害后果。

原始出处：

Erin S. Coyne, Nathalie Bédard, Ying Jia Gong, The deubiquitinating enzyme USP19 modulates adipogenesis and potentiates high-fat-diet-induced obesity and glucose intolerance in mice

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2019-07-27 ms9608593228839890

#DIA#

29 0
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2019-12-01 ms5439512287675881

#BET#

28 0
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2019-04-09 ms5906905816781247

#饮食诱导#

28 0
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2019-04-06 pcw111

#高脂#

28 0
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2019-04-04 天地飞扬

了解一下，谢谢分享！

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DIABETOLOGIA：去泛素酶USP19可调节小鼠的脂肪生成，增强高脂饮食诱导的肥胖和葡萄糖耐受不良

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