Visfain has been extensively studied in mammals and has been shown to play an important role in obesity and insulin resistance. However, there is a paucity of information on visfatin regulation in non-mammalian species. After characterization of chicken visfatin gene, we undertook this study to determine its hormonal regulation in avian (non-mammalian) liver cells. Addition of 5 ng/mL TNFα, 100 ng/mL leptin, 1, 3, 10 or 100 ng/mL T3 for 24 h upregulated visfatin gene expression by 1.2, 1.8, 1.95, 1.75, 1.80, and 2.45 folds (P < .05), respectively, compared to untreated LMH cells. Administration of 10 ng/mL of orexin A significantly down regulated visfatin gene expression by 1.35 folds compared to control cells. In contrast, treatment with IL-6 or orexin B for 24 h did not influence visfatin mRNA abundance. These pro-inflammatory cytokines and obesity-related hormones modulate the expression of CRP, INSIG2, and nuclear orphan receptors. Hepatic CRP gene expression was significantly upregulated by IL-6, TNFα, orexin B, and T3 and down regulated by leptin and orexin A. LXR mRNA abundances were increased by orexin A, decreased by orexin B, and T3, and did not affected by IL6, TNFα, or leptin. The expression of FXR gene was induced by IL-6, leptin, and T3, but it was not influenced by TNFα, orexin A or B. CXR gene expression was up regulated by TNFα, leptin, orexin B, and T3, down regulated by 5 ng/mL orexin A, and did not affected by IL-6. INSIG2 mRNA levels were increased by TNFα (5 ng/mL), leptin (100 ng/mL), and T3 (1, 3, 10, and 100 ng/mL), decreased by orexin A, and remained unchanged with IL-6 or orexin B treatment. Together, this is the first report showing hormonal regulation of visfatin in avian hepatocyte cells and suggesting a potential role of CRP, INSIG2, and nuclear orphan receptor LXR, FXR, and CXR in mediating these hormonal effects.

中文翻译：

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visfatin基因在禽来克霍恩男性肝癌（LMH）细胞中的激素调节。

Visfain已在哺乳动物中进行了广泛研究，已显示在肥胖症和胰岛素抵抗中起重要作用。但是，关于非哺乳动物物种中visfatin调控的信息很少。表征鸡visfatin基因后，我们进行了这项研究，以确定其在禽类（非哺乳动物）肝细胞中的激素调节。添加5 ng / mLTNFα，100 ng / mL瘦蛋白，1、3、10或100 ng / mL T3 24小时可将visfatin基因表达上调1.2、1.8、1.95、1.75、1.80和2.45倍（P <。 05）分别与未处理的LMH细胞进行比较。与对照细胞相比，给予10 ng / mL的orexin A显着下调了visfatin基因的表达1.35倍。相反，用IL-6或orexin B处理24小时不影响visfatin mRNA的丰度。这些促炎性细胞因子和肥胖相关激素调节CRP，INSIG2和核孤儿受体的表达。肝CRP基因表达被IL-6，TNFα，orexin B和T3显着上调，而被瘦素和orexin A所下调。orexinA增加LXR mRNA的丰度，orexin B和T3降低LXR mRNA的丰度，并且不受L3R的影响IL6，TNFα或瘦素。FXR基因的表达受IL-6，瘦素和T3的诱导，但不受TNFα，orexin A或B的影响。CXR基因表达受TNFα，leptin，orexin B和T3的上调，而受TNFα，leptin和T3的下调。 5 ng / mL的orexin A，不受IL-6的影响。TNFα（5 ng / mL），瘦素（100 ng / mL）和T3（1、3、10和100 ng / mL）增加了INSIG2 mRNA的水平，而orexin A降低了INSIG2的水平，而IL-6则保持不变或食欲素B治疗。一起，