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首页> 外文期刊>BMC Veterinary Research >Fibroblast growth factor-1 as a mediator of paracrine effects of canine adipose tissue-derived mesenchymal stem cells on in vitro-induced insulin resistance models
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Fibroblast growth factor-1 as a mediator of paracrine effects of canine adipose tissue-derived mesenchymal stem cells on in vitro-induced insulin resistance models

机译：成纤维细胞生长因子-1介导犬脂肪组织间充质干细胞对体外诱导的胰岛素抵抗模型的旁分泌作用

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In the field of diabetes research, many studies on cell therapy have been conducted using mesenchymal stem cells. This research was intended to shed light on the influence of canine adipose-tissue-derived mesenchymal stem cell conditioned medium (cAT-MSC CM) on in vitro insulin resistance models that were induced in differentiated 3T3-L1 adipocytes and the possible mechanisms involved in the phenomenon. Gene expression levels of insulin receptor substrate-1 (IRS-1) and glucose transporter type 4 (GLUT4) were used as indicators of insulin resistance. Relative protein expression levels of IRS-1 and GLUT4 were augmented in the cAT-MSC CM treatment group compared to insulin resistance models, indicating beneficial effects of cAT-MSC to DM, probably by actions of secreting factors. With reference to previous studies on fibroblast growth factor-1 (FGF1), we proposed FGF1 as a key contributing factor to the mechanism of action. We added anti-FGF1 neutralizing antibody to the CM-treated insulin resistance models. As a result, significantly diminished protein levels of IRS-1 and GLUT4 were observed, supporting our assumption. Similar results were observed in glucose uptake assay. Accordingly, this study advocated the potential of FGF-1 from cAT-MSC CM as an alternative insulin sensitizer and discovered a signalling factor associated with the paracrine effects of cAT-MSC.
机译：在糖尿病研究领域，已经使用间充质干细胞进行了许多细胞治疗研究。这项研究旨在阐明犬脂肪组织间充质干细胞条件培养基（cAT-MSC CM）对分化的3T3-L1脂肪细胞诱导的体外胰岛素抵抗模型的影响以及可能的机制现象。胰岛素受体底物1（IRS-1）和4型葡萄糖转运蛋白（GLUT4）的基因表达水平被用作胰岛素抵抗的指标。与胰岛素抵抗模型相比，cAT-MSC CM治疗组中IRS-1和GLUT4的相对蛋白表达水平增加，表明cAT-MSC对DM的有益作用可能是分泌因子的作用。参考先前对成纤维细胞生长因子1（FGF1）的研究，我们提出FGF1是作用机制的关键促成因素。我们在CM治疗的胰岛素抵抗模型中添加了抗FGF1中和抗体。结果，观察到IRS-1和GLUT4的蛋白质水平显着降低，支持了我们的假设。在葡萄糖摄取测定中观察到相似的结果。因此，这项研究提倡了来自cAT-MSC CM的FGF-1作为替代胰岛素增敏剂的潜力，并发现了与cAT-MSC旁分泌作用相关的信号转导因子。

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