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首页> 美国卫生研究院文献>International Journal of Molecular Sciences >Testosterone Deficiency Induces Changes of the Transcriptomes of Visceral Adipose Tissue in Miniature Pigs Fed a High-Fat and High-Cholesterol Diet
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Testosterone Deficiency Induces Changes of the Transcriptomes of Visceral Adipose Tissue in Miniature Pigs Fed a High-Fat and High-Cholesterol Diet

机译：睾丸激素缺乏症诱发高脂高胆固醇饮食的小型猪内脏脂肪组织转录组的变化

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Testosterone deficiency causes fat deposition, particularly in visceral fat, and its replacement might reverse fat accumulation, however, the underlying mechanisms of such processes under diet-induced adiposity are largely unknown. To gain insights into the genome-wide role of androgen on visceral adipose tissue (VAT), RNA-Seq was used to investigate testosterone deficiency induced changes of VAT in miniature pigs fed a high-fat and high-cholesterol (HFC) diet among intact male pigs (IM), castrated male pigs (CM), and castrated male pigs with testosterone replacement (CMT) treatments. The results showed that testosterone deficiency significantly increased VAT deposition and serum leptin concentrations. Moreover, a total of 1732 differentially expressed genes (DEGs) were identified between any two groups. Compared with gene expression profiles in IM and CMT pigs, upregulated genes in CM pigs, i.e., LOC100520753 (CD68), LCN2, EMR1, S100A9, NCF1 (p47phox), and LEP, were mainly involved in inflammatory response, oxidation-reduction process, and lipid metabolic process, while downregulated genes in CM pigs, i.e., ABHD5, SPP1, and GAS6, were focused on cell differentiation and cell adhesion. Taken together, our study demonstrates that testosterone deficiency alters the expression of numerous genes involved in key biological processes of VAT accumulation under HFC diet and provides a novel genome-wide view on the role of androgen on VAT deposition under HFC diet, thus improving our understanding of the molecular mechanisms involved in VAT changes induced by testosterone deficiency.
机译：睾丸激素缺乏会引起脂肪沉积，尤其是在内脏脂肪中的脂肪沉积，其替代可能会逆转脂肪的积累，但是，在饮食诱导的肥胖症下，这种过程的潜在机制尚不清楚。为了深入了解雄激素在全基因组内脏脂肪组织（VAT）上的全基因组作用，使用RNA-Seq研究睾丸激素缺乏引起的饲喂高脂高胆固醇（HFC）日粮的小型猪中VAT的变化雄性猪（IM），去势雄性猪（CM）和去势雄性猪进行睾丸激素替代（CMT）处理。结果表明，睾丸激素缺乏显着增加了VAT沉积和血清瘦素浓度。此外，在任意两组之间总共鉴定出1732个差异表达基因（DEG）。与IM和CMT猪的基因表达谱相比，CM猪的上调基因，即LOC100520753（CD68），LCN2，EMR1，S100A9，NCF1（p47phox）和LEP，主要参与炎症反应，氧化还原过程，脂代谢过程和脂代谢过程虽然被下调，但CM猪的基因ABHD5，SPP1和GAS6却集中在细胞分化和细胞粘附上。综上所述，我们的研究表明，睾丸激素缺乏症会改变HFC饮食下增值税积累关键生物学过程中涉及的许多基因的表达，并为HFC饮食下雄激素在VAT沉积中的作用提供全基因组新观点，从而增进了我们的理解。睾丸激素缺乏引起的增值税变化的分子机制研究

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