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首页> 外文期刊>Molecular and Cellular Endocrinology >Triiodothyronine activated extranuclear pathways upregulate adiponectin and leptin in murine adipocytes
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Triiodothyronine activated extranuclear pathways upregulate adiponectin and leptin in murine adipocytes

机译:三碘罗酮激活的外耳扫描途径上调牛肾脂肪细胞中的脂联素和瘦素

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摘要

Adiponectin and leptin, important for metabolic regulation, are synthesized and secreted by adipose tissue and are influenced by triiodothyronine (T3) that activates the MAPK/ERK and integrin alpha V beta 3 pathways, modulating gene expression. Adipocytes were treated with T3 (10 nM), for 1 h, in the absence or presence of PD98059 (PD) and tetraiodothyroacetic acid (Tetrac), which are pathways inhibitors. The cells were incubated with Adipo Red/Oil Red O reagents, and intracellular lipid accumulation [glycerol and triacylglycerol (TAG)], MTT, 8-hydroxideoxyguanosine (8-OH-dG), and mRNA and protein expression were assessed. T3 increased leptin mRNA and protein expression, and, in contrast, there was a decrease in the Tetrac + T3 group. Adiponectin mRNA expression was not altered by T3, though it had increased its protein expression, which was terminated by inhibitors PD + T3 and Tetrac + T3. However, T3 did not alter PPAR gamma protein expression, lipid accumulation, TAG, glycerol, and DNA damage, but PD + T3 and Tetrac + T3 reduced these parameters. T3 activated the MAPK/ERK pathway on adipocytes to modulate the adiponectin protein expression and integrin alpha V beta 3 to alter the leptin gene expression.
机译:脂联素和瘦素对代谢调节重要的是由脂肪组织合成和分泌的,并受三碘甲苯酮(T3)的影响,其激活MAPK / ERK和整合素αVβ3途径,调节基因表达。在PD98059(Pd)和四碘乙酸(Tetrac)的不存在或存在下,用T3(10nm),1小时处理脂肪细胞,其是途径抑制剂。将细胞与Adipo Red / Oil Red O试剂一起温育,并且细胞内脂质积累烷化液α,MTT,8-羟基氧羰基(8-OH-DG)和mRNA和蛋白表达进行评估。 T3增加瘦素mRNA和蛋白质表达,并且相比之下,TETRAC + T3基团有降低。脂联素mRNA表达未通过T3改变,尽管它增加了其蛋白质表达,其被抑制剂PD + T3和TETRAC + T3终止。然而,T3没有改变PPARγ蛋白表达,脂质积累,标签,甘油和DNA损伤,但Pd + T3和Tetrac + T3减少了这些参数。 T3在脂肪细胞上激活MAPK / ERK途径以调节脂联蛋白表达并整合αVβ3以改变瘦素基因表达。

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