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 αVβ3 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 PPARγ 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 αvβ3 to alter the leptin gene expression.

中文翻译：

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Triiodothyronine激活的核外通路上调了小鼠脂肪细胞中的脂联素和瘦素。

脂联素和瘦素对于代谢调节很重要，由脂肪组织合成和分泌，并受激活MAPK / ERK和整联蛋白αVβ3途径的三碘甲状腺素（T3）的影响，从而调节基因表达。在不存在或不存在PD98059（PD）和四碘胸苷乙酸（Tetrac）的情况下，用T3（10 nM）处理脂肪细胞1 h。将细胞与Adipo Red / Oil Red O试剂一起孵育，并测量细胞内脂质蓄积[甘油和三酰基甘油（TAG）]，MTT，8-羟氧基鸟苷（8-OH-dG），并评估mRNA和蛋白质表达。T3增加瘦素mRNA和蛋白质表达，相反，Tetrac + T3组减少。脂联素mRNA的表达并未被T3改变，尽管它增加了其蛋白表达，它被抑制剂PD + T3和Tetrac + T3终止。然而，T3并没有改变PPARγ蛋白的表达，脂质蓄积，TAG，甘油和DNA损伤，但PD + T3和Tetrac + T3降低了这些参数。T3激活脂肪细胞上的MAPK / ERK途径以调节脂联素蛋白表达，并整合素αvβ3改变瘦素基因表达。