Department of Human Anatomy and Histology, Tianjin Medical University, Tianjin 300070, P.R. China.
Key Laboratory of Hormones and Development (Ministry of Health), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Metabolic Diseases Hospital and Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin 300070, P.R. China.
Mol Med Rep. 2018 Mar;17(3):4499-4507. doi: 10.3892/mmr.2018.8438. Epub 2018 Jan 16.
Liraglutide, as a glucagon-like peptide‑1 analogue, is used to treat type 2 diabetes mellitus and obesity. Previous findings have demonstrated the effects of liraglutide on adipogenesis; however, the underlying mechanism involved in this process remains to be elucidated. In the present study, to certify the effect of liraglutide on adipogenesis and explore the possible underlying mechanism involved in this process, preadipocyte 3T3‑L1 cells were cultured in adipocyte‑inducing medium and treated with liraglutide. Subsequently, the expression levels of the master transcription factors and adipocyte‑specific genes were measured by reverse transcription‑quantitative polymerase chain reaction and immunoblotting analysis. Lipid droplet production was detected by Oil red O staining. Cell proliferation was determined by a Cell Counting Kit-8 assay and cell immunofluorescence for Ki67, and apoptosis was assessed by flow cytometry. Next, the expression levels of the core components in the Hippo‑yes‑associated protein (YAP) signaling pathway as well as YAP‑specific target genes were measured. Finally, short interfering RNAs of mammalian ste20 kinase 1/2 (MST1/2), a key protein kinase in the Hippo‑YAP pathway, were used to determine whether liraglutide regulated adipogenic differentiation via the Hippo‑YAP pathway. It was demonstrated that liraglutide promoted adipogenic differentiation, suppressed proliferation, did not affect apoptosis of 3T3‑L1 cells and activated the Hippo‑YAP signaling pathway at the initial stage of adipogenesis. Silencing of MST1 counteracted the effect of increasing adipogenesis by liraglutide. These results suggested that liraglutide may activate the Hippo‑YAP signaling pathway leading to the inhibition of proliferation of preadipocyte 3T3‑L1 cells, and result in cells achieving transformation into mature adipocytes sooner. Taken together, the results of the present study may expand knowledge of the underlying mechanism of liraglutide facilitating adipogenesis, and may contribute to the development of GLP‑1 receptor agonists for weight loss and increased insulin sensitivity.
利拉鲁肽是一种胰高血糖素样肽-1 类似物,用于治疗 2 型糖尿病和肥胖症。先前的研究结果表明,利拉鲁肽可影响脂肪生成;然而,其涉及的具体作用机制仍有待阐明。在本研究中,为了验证利拉鲁肽对脂肪生成的影响,并探索该过程中可能涉及的潜在机制,将前脂肪细胞 3T3-L1 细胞在脂肪细胞诱导培养基中培养,并使用利拉鲁肽进行处理。随后,通过逆转录-定量聚合酶链反应和免疫印迹分析测定主转录因子和脂肪细胞特异性基因的表达水平。通过油红 O 染色检测脂滴生成。通过细胞计数试剂盒-8 测定法和 Ki67 的细胞免疫荧光法测定细胞增殖,通过流式细胞术评估细胞凋亡。接下来,测定 Hippo-Yes 相关蛋白 (YAP) 信号通路的核心成分以及 YAP 特异性靶基因的表达水平。最后,使用哺乳动物 STE20 激酶 1/2 (MST1/2) 的短发夹 RNA(一种 Hippo-YAP 通路中的关键蛋白激酶)确定利拉鲁肽是否通过 Hippo-YAP 通路调节脂肪生成分化。结果表明,利拉鲁肽促进脂肪生成分化,抑制增殖,不影响 3T3-L1 细胞的凋亡,并且在脂肪生成的初始阶段激活 Hippo-YAP 信号通路。沉默 MST1 可拮抗利拉鲁肽增加脂肪生成的作用。这些结果表明,利拉鲁肽可能激活 Hippo-YAP 信号通路,从而抑制前脂肪细胞 3T3-L1 细胞的增殖,导致细胞更早地向成熟脂肪细胞转化。综上所述,本研究的结果可能扩展了利拉鲁肽促进脂肪生成的潜在机制的相关知识,并可能有助于开发 GLP-1 受体激动剂以实现减肥和增加胰岛素敏感性。