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首页> 外文期刊>Experimental and clinical endocrinology and diabetes: Official journal, German Society of Endocrinology [and] German Diabetes Association >Inflammatory markers and adipokines alter adipocyte-derived ASP production through direct and indirect immune interaction
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Inflammatory markers and adipokines alter adipocyte-derived ASP production through direct and indirect immune interaction

机译：炎症标志物和脂肪因子通过直接和间接的免疫相互作用改变脂肪细胞的ASP产生

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摘要

Obesity and related metabolic diseases are associated with chronic low-grade inflammation, characterized by increased pro-inflammatory proteins. Several studies have demonstrated increases in acylation stimulating protein (ASP) and its precursor protein C3 in obesity, diabetes and dyslipidemia. To evaluate the effects of acute inflammatory factors and adipokines on ASP production and potential mechanisms of action, 3T3-L1 adipocytes were treated for 24 h with adipokines, cytokines, macrophage-conditioned media and direct co-culture with J774 macrophages. ASP and C3 in the media were evaluated in relation to changes in adipocyte lipid metabolism (cellular triglyceride stores). Leptin, adiponectin, IL-10, LPS and TNF-α increased ASP production (151%, 153%, 190%, 318%, 134%, P<0.05, respectively,). C5a and RANTES (Regulated and normal T cell expressed and secreted) decreased ASP production (- 34%, - 47%, P<0.05), which was also associated with a decrease in the precursor protein C3 (- 39% to - 51%, P<0.01), while keratinocyte chemoattractant (KC; murine IL-8 ortholog) had no effect on ASP and C3 secretion. By contrast, apelin, omentin and visfatin also decreased ASP (- 27%, - 49%, - 22%, P<0.05), but without changes in precursor protein C3 secretion. Macrophage-conditioned media alone had little effect on C3 or ASP, while co-culture of adipocytes with macrophages markedly increased ASP and C3 production (272%, 167%, P<0.05). These in vitro results suggest various metabolic hormones and inflammatory factors can affect ASP production through increased precursor C3 production and/or by changing the rate of C3 conversion to ASP. As an adipokine, ASP could constitute a new link between adipocytes and macrophages.
机译：肥胖症和相关的代谢性疾病与慢性低度炎症相关，其特征在于促炎蛋白增加。几项研究表明，肥胖症，糖尿病和血脂异常时酰化刺激蛋白（ASP）及其前体蛋白C3含量增加。为了评估急性炎症因子和脂肪因子对ASP产生和潜在作用机制的影响，将3T3-L1脂肪细胞与脂肪因子，细胞因子，巨噬细胞条件培养基一起处理24小时，并与J774巨噬细胞直接共培养。评估培养基中的ASP和C3与脂肪细胞脂质代谢（细胞甘油三酯库）变化的关系。瘦素，脂联素，IL-10，LPS和TNF-α增加ASP产量（分别为151％，153％，190％，318％，134％，P <0.05）。 C5a和RANTES（表达和分泌正常和正常T细胞）降低ASP产量（-34％，-47％，P <0.05），这也与前体蛋白C3的降低（-39％至-51％）有关，P <0.01），而角质形成细胞趋化因子（KC;鼠IL-8直系同源物）对ASP和C3分泌没有影响。相比之下，apelin，omentin和visfatin也降低了ASP（-27％，-49％，-22％，P <0.05），但前体蛋白C3分泌没有变化。单独的巨噬细胞条件培养基对C3或ASP几乎没有影响，而脂肪细胞与巨噬细胞的共培养显着提高了ASP和C3的产生（272％，167％，P <0.05）。这些体外结果表明，各种代谢激素和炎性因子可通过增加前体C3的产生和/或通过改变C3转化为ASP的速率来影响ASP的产生。作为脂肪因子，ASP可能构成脂肪细胞和巨噬细胞之间的新纽带。

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