Suppressor of cytokine signaling 2 (SOCS2) plays an important role in fat deposition, skeletal muscle, central nervous system development, and mitochondria biogenesis. Nevertheless, the regulatory mechanisms of SOCS2 on mitochondrial fatty acid oxidation (FAO) remain unclear. Leptin could inhibit food intake and increase thermogenesis through leptin receptor (LepR), which was present in the hypothalamus and certain peripheral organs, including adipose tissue. With strong interest, we focused on the connection between leptin and SOCS2 and their effect on FAO in adipocytes. In our study, we found that the mRNA level of SOCS2 and the protein levels of PGC-1α, CPT-1b, FAT, and p-ACC were elevated by leptin in the inguinal adipose tissue of mice. On the contrary, the protein levels of FABP4, FATP1, and FAS were declined. The genes related to fatty acid oxidation such as PGC-1α, NRF-1, TFAM, CPT-1b, AOX1, COX2, and UCP2 were attenuated by SOCS2, but elevated by leptin. Moreover, fatty acid oxidation enzyme MCAD, LCAD, and Cyt C levels were reduced in response to SOCS2. These reductions correspond well with the reduced release of free fatty acid and the reduction of mitochondrial complexes I and III by SOCS2. Furthermore, JAK2/AMPK pathway-specific inhibitors could block the mitochondrial FAO; hence, this pathway was implied to have a potential impact on FAO. Together, these studies suggested that SOCS2 had a negative effect on mitochondrial fatty acid oxidation, and the LepR/JAK2/AMPK pathway played a crucial role in this process.

中文翻译：

---

SOCS2通过抑制小鼠脂肪细胞中的LepR / JAK2 / AMPK信号通路抑制线粒体脂肪酸氧化。

细胞因子信号传导抑制因子2（SOCS2）在脂肪沉积，骨骼肌，中枢神经系统发育和线粒体生物发生中起重要作用。然而，SOCS2对线粒体脂肪酸氧化（FAO）的调控机制仍不清楚。瘦素可抑制食物摄取并通过瘦素受体（LepR）促进生热，瘦素受体存在于下丘脑和某些外围器官，包括脂肪组织中。我们怀着浓厚的兴趣，专注于瘦素和SOCS2之间的联系及其对脂肪细胞中FAO的影响。在我们的研究中，我们发现SOCS2的mRNA水平和PGC- 1α的蛋白水平瘦素在小鼠腹股沟脂肪组织中升高了CPT-1b，FAT和p-ACC的表达。相反，FABP4，FATP1和FAS的蛋白质水平下降。与脂肪酸氧化有关的基因，例如PGC- 1α，NRF-1，TFAM，CPT-1b，AOX1，COX2和UCP2被SOCS2减弱，但被瘦素升高。此外，响应SOCS2，脂肪酸氧化酶MCAD，LCAD和Cyt C水平降低。这些减少与SOCS2减少的游离脂肪酸释放以及线粒体复合物I和III的减少非常吻合。此外，JAK2 / AMPK途径特异性抑制剂可能会阻断线粒体FAO。因此，暗示该途径会对粮农组织产生潜在影响。总之，这些研究表明，SOCS2对线粒体脂肪酸氧化具有负面影响，并且LepR / JAK2 / AMPK途径在该过程中起着至关重要的作用。