C1q/TNF-related protein 4 (CTRP4) has been reported to decrease food intake and regulate energy homeostasis. However, its underlying mechanism and signaling pathway remain unknown. Using an adenovirus-mediated hypothalamic CTRP4 overexpression model, we investigated the impact of CTRP4 on food intake and signal transducer and activator of transcription 3 (STAT3) signaling pathway in normal chow-fed mice. Expressions of neuropeptides including proopiomelanocortin (POMC) and neuropeptide Y (NPY) were studied in hypothalamus by Western blot and immunochemistry. STAT3 and suppressor of cytokine signaling 3 (SOCS3) were determined by Western blot. STAT3 signaling pathway was also investigated in Neuro 2A (N2a) cells after CTRP4 overexpression intervention. We found that food intake decreased significantly in mice under normal chow condition after CTRP4 overexpression. Both immunohistochemistry and Western blot demonstrated that POMC expression was significantly increased while NPY expression was significantly decreased. The changes of neuropeptides were accompanied by significant increased STAT3 phosphorylation and decreased SOCS3 levels. The same changes of neuropeptides and STAT3 signaling were also found in N2a cells after CTRP4 overexpression intervention. Collectively, our data reveals that CTRP4 induces the activation of STAT3 signaling and decreases food intake.

中文翻译：

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C1q/TNF 相关蛋白 4 诱导信号转导和转录 3 通路激活剂并调节食物摄入。

据报道，C1q/TNF 相关蛋白 4 (CTRP4) 可减少食物摄入并调节能量稳态。然而，其潜在机制和信号通路仍然未知。使用腺病毒介导的下丘脑 CTRP4 过表达模型，我们研究了 CTRP4 对正常食物喂养小鼠食物摄入和信号转导和转录激活因子 3 (STAT3) 信号通路的影响。通过蛋白质印迹和免疫化学研究了包括阿片黑皮质素原 (POMC) 和神经肽 Y (NPY) 在内的神经肽在下丘脑中的表达。通过蛋白质印迹测定 STAT3 和细胞因子信号 3 (SOCS3) 抑制因子。在 CTRP4 过表达干预后，还在 Neuro 2A (N2a) 细胞中研究了 STAT3 信号通路。我们发现 CTRP4 过表达后，正常食物条件下小鼠的食物摄入量显着减少。免疫组化和Western印迹均显示POMC表达显着增加，而NPY表达显着降低。神经肽的变化伴随着STAT3磷酸化显着增加和SOCS3水平降低。CTRP4过表达干预后，在N2a细胞中也发现了相同的神经肽和STAT3信号变化。总的来说，我们的数据显示 CTRP4 诱导 STAT3 信号的激活并减少食物摄入。神经肽的变化伴随着STAT3磷酸化显着增加和SOCS3水平降低。CTRP4过表达干预后，在N2a细胞中也发现了相同的神经肽和STAT3信号变化。总的来说，我们的数据显示 CTRP4 诱导 STAT3 信号的激活并减少食物摄入。神经肽的变化伴随着STAT3磷酸化显着增加和SOCS3水平降低。CTRP4过表达干预后，在N2a细胞中也发现了相同的神经肽和STAT3信号变化。总的来说，我们的数据显示 CTRP4 诱导 STAT3 信号的激活并减少食物摄入。