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The roles of adipokines, proinflammatory cytokines, and adipose tissue macrophages in obesity-associated insulin resistance have been explored in both animal and human studies. However, our current understanding of obesity-associated insulin resistance relies on studies of artificial metabolic extremes. The purpose of this study was to explore the roles of adipokines, proinflammatory cytokines, and adipose tissue macrophages in human patients with modest obesity and early metabolic dysfunction. We obtained omental adipose tissue and fasting blood samples from 51 females undergoing gynecologic surgery. We investigated serum concentrations of proinflammatory cytokines and adipokines as well as the mRNA expression of proinflammatory and macrophage phenotype markers in visceral adipose tissue using ELISA and quantitative RT-PCR. We measured adipose tissue inflammation and macrophage infiltration using immunohistochemical analysis. Serum levels of adiponectin and leptin were significantly correlated with HOMA-IR and body mass index. The levels of expression of MCP-1 and TNF-α in visceral adipose tissue were also higher in the obese group (body mass index ≥ 25). The expression of mRNA MCP-1 in visceral adipose tissue was positively correlated with body mass index (r = 0.428, p = 0.037) but not with HOMA-IR, whereas TNF-α in visceral adipose tissue was correlated with HOMA-IR (r = 0.462, p = 0.035) but not with body mass index. There was no obvious change in macrophage phenotype or macrophage infiltration in patients with modest obesity or early metabolic dysfunction. Expression of mRNA CD163/CD68 was significantly related to mitochondrial-associated genes and serum inflammatory cytokine levels of resistin and leptin. These results suggest that changes in the production of inflammatory biomolecules precede increased immune cell infiltration and induction of a macrophage phenotype switch in visceral adipose tissue. Furthermore, serum resistin and leptin have specific roles in the regulation of adipose tissue macrophages in patients with modest obesity or early metabolic dysfunction.  相似文献   

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彭颗红  薛敏  肖松舒 《生物磁学》2009,(13):2514-2516,2537
目的:探讨visfatin基因在多囊卵巢综合征(PCOS)网膜脂肪组织中的表达及相关影响因素。方法:采用半定量RT-PCR方法检测PCOS组(30例)和对照组(25例)网膜脂肪组织visfatin mRNA表达,并测量体重指数、腰臀比、空腹血糖、空腹胰岛素、胰岛素抵抗指数和血清性激素水平。结果:①PCOS组网膜脂肪组织visfatin mRNA表达量高于对照组(P=0.000)。②网膜脂肪组织visfatin mRNA的表达量与BMI、WHR、FINS、HOMA-IR呈正相关(P〈0.05)。③多元逐步回归分析显示,HOMA-IR(P=0.000)和WHR(P=0.005)是影响网膜脂肪组织visfatin mRNA表达的相关因素。结论:网膜脂肪组织visfatin mRNA表达可能与PCOS胰岛素抵抗的发生和肥胖相关。  相似文献   

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近年来的研究发现,生物体内存在着大量的非编码RNA(non.codingRNAs,ncRNA),它们在染色质修饰、基因转录、RNA剪接和mRNA翻译等多种水平上参与了基因表达的调控。ncRNA中的小分子RNA如miRNA能够识别特定的目标mRNA,通过与mRNAs3’非翻译区结合,影响mRNA转录及蛋白质翻译;siRNA是RNA干扰的引发物,能够导致与dsRNA同源的mRNA降解,进而抑制相应基因表达;saRNA是目前最新发现的一种靶向目的基因启动子区的在转录水平激活目的基因表达的dsRNA。miRNA、siRNA和saRNA在生成机制、作用途径等方面关系密切,既区别又相互联系,小分子RNA的研究将是今后分子生物学的研究热点之一。  相似文献   

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