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Identification of novel adipokines differential regulated in C57BL/Ks and C57BL/6

机译:鉴定在C57BL / Ks和C57BL / 6中受调控的新型脂肪因子

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Visceral adiposity is associated with metabolic disorders, but little is known on the underlying pathophysiological mechanism. One possible link might be the release of various signalling and mediator proteins, named adipokines. Our hypothesis was that dependent on genetic background factors are released which might trigger a primary disease susceptibility. This study characterizes the adipokines released from visceral adipose tissue from two metabolic healthy mouse strains, i.e. C57BL/Ks (BKS) and C57BL/6 (C57), of which the former genetic background is more sensitive to develop diabetes following metabolic challenge. Using liquid chromatography (LC)-electrospray ionization (ESI)-MS/MS, a reference map comprising 597 adipokines was generated (http://www.diabesityprot.org). Thirty-five adipokines, including six not previously described ones, were differentially released between the mouse strains. Most notable is the reduced release of the adiponectin-binding protein T-Cadherin (CAD13) in BKS mice. This observation highlights the importance of secretome profiling in unravelling the complex interplay between genetic diversity and lifestyle.
机译:内脏脂肪代谢与代谢紊乱有关,但对潜在的病理生理机制知之甚少。一种可能的联系可能是释放多种信号传导和介体蛋白,称为脂肪因子。我们的假设是依赖遗传背景因素的释放可能会触发原发性疾病的易感性。这项研究的特征是从两种代谢健康小鼠品系C57BL / Ks(BKS)和C57BL / 6(C57)的内脏脂肪组织释放的脂肪因子,其前遗传背景对代谢挑战后的糖尿病更敏感。使用液相色谱(LC)-电喷雾电离(ESI)-MS / MS,生成了包含597种脂肪因子的参考图谱(http://www.diabesityprot.org)。在小鼠品系之间有差别地释放了35种脂肪因子,其中包括6种先前未描述的脂肪因子。最值得注意的是BKS小鼠中脂联素结合蛋白T-钙黏着蛋白(CAD13)的释放减少。该观察结果突出了分泌组图谱分析在阐明遗传多样性与生活方式之间复杂相互作用方面的重要性。

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