de Oliveira Miriane, Rodrigues Bruna Moretto, Olimpio Regiane Marques Castro, Mathias Lucas Solla, De Sibio Maria Teresa, Moretto Fernanda Cristina Fontes, Graceli Jones Bernardes, Nogueira Célia Regina
Department of Internal Medicine, Botucatu Medicine School, São Paulo State University (UNESP), Prof. Mário Rubens Guimarães Montenegro Avenue, s/n Bairro: UNESP - Campus de Botucatu 18618687 - Botucatu, SP, Brazil.
Department of Morphology, Federal University of Espírito Santo, Marechal Campos Avenue, 1468, Prédio do básico I, sala 5, 29043-090 Vitória, ES, Brazil.
Lipids. 2019 Feb;54(2-3):133-140. doi: 10.1002/lipd.12135.
Adipose tissue (AT), an endocrine organ that modulates several physiological functions by synthesizing and releasing adipokines such as adiponectin, is a metabolic target of triiodothyronine (T3). T3 and adiponectin play important roles in controlling normal metabolic functions such as stimulation of fatty acid oxidation and increase in thermogenesis. The phosphatidylinositol 3-kinase (PI3K) pathway is important for the differentiation of preadipocytes into adipocytes and can be activated by T3 for the transcription of specific genes, such as adiponectin. We examined the role of PI3K in adiponectin modulation by T3 action in murine adipocytes (3T3-L1). The 3T3-L1 adipocytes were treated with 1000 nM T3 for 1 h in the presence or absence of 50 μM LY294002 (LY), a PI3K inhibitor. Then, we assessed the expression of adiponectin and the phosphorylated serine/threonine kinase Akt (pAkt), a PI3K signaling protein, in the adipocytes. Adiponectin and pAKT levels were higher in the T3-adipocyte cells, whereas in the LY group adiponectin was elevated and pAKT was decreased compared to the control (C). PI3K pathway inhibition for 1 h and posterior treatment with T3, in LY + T3, reduced the adiponectin level and increased pAKT levels compared to those in LY. T3 stimulated adiponectin levels by PI3K pathway activation and T3 can compensate alteration in the PI3K pathway, because with inhibition of the pathway it is able to maintain the basal levels of adiponectin and pAKT.
脂肪组织（AT）是一种内分泌器官，通过合成和释放脂联素等脂肪因子来调节多种生理功能，它是三碘甲状腺原氨酸（T3）的代谢靶点。T3和脂联素在控制正常代谢功能（如刺激脂肪酸氧化和增加产热）中发挥重要作用。磷脂酰肌醇3激酶（PI3K）通路对于前脂肪细胞分化为脂肪细胞很重要，并且可以被T3激活以促进特定基因（如脂联素）的转录。我们研究了PI3K在T3对小鼠脂肪细胞（3T3-L1）脂联素调节中的作用。在存在或不存在50μM LY294002（LY，一种PI3K抑制剂）的情况下，将3T3-L1脂肪细胞用1000 nM T3处理1小时。然后，我们评估了脂肪细胞中脂联素的表达以及PI3K信号蛋白磷酸化丝氨酸/苏氨酸激酶Akt（pAkt）的水平。T3处理的脂肪细胞中脂联素和pAKT水平较高，而在LY组中，与对照组（C）相比，脂联素升高而pAKT降低。在LY + T3组中，PI3K通路抑制1小时后再用T3处理，与LY组相比，脂联素水平降低而pAKT水平升高。T3通过激活PI3K通路刺激脂联素水平，并且T3可以补偿PI3K通路的改变，因为在该通路受到抑制时，它能够维持脂联素和pAKT的基础水平。
