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胰高血糖素样肽_1的研究进展_赵伟
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内容提示：胰高血糖素样肽_1的研究进展_赵伟,胰高血糖素,胰高血糖素的靶细胞,胰高血糖素类多肽,注射用胰激肽原酶,胰激肽,胰激肽原酶肠溶片,胰激肽原酶,胰肽糖消,胰激肽原酶注射液,胰功肽试验
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作者：Beyond
来源：生物谷
关键词：胰高血糖素样肽1,STAT3,巨噬细胞,极化
据了解，胰高血糖素样肽1（GLP-1）是餐后从小肠L型细胞分泌的一种具有调节葡萄糖稳态功能的激素。
目前，GLP-1已被用于的治疗，主要原因是其对胰岛素抵抗具有有益作用。许多类型的细胞包括巨噬细胞都表达GLP-1受体（GLP-1R），GLP-1通过抑制巨噬细胞功能，进而抑制动脉粥样硬化的发展。
然而，迄今为止有关GLP-1/GLP-1R信号在巨噬细胞活化中的作用相关研究很少。在一项最新研究中，科研人员探讨了GLP-1和艾塞那肽(Exenatide) 对人单核细胞源性巨噬细胞（HMDM）激活的作用，艾塞那肽是GLP-1R激动剂，是首个化学全合成的肠促胰岛素类似物，可降低2型患者的空腹和餐后血糖。
研究发现，GLP-1诱导转录因子3（STAT3）活化激活的信号转导。GLP-1R沉默后能抑制GLP-1诱导的STAT3活化。此外，激活型（M2）巨噬细胞相关的分子如IL-1、CD163等在接受GLP刺激后都显著上调。
此外， GLP-1处理共培养的RAW3T3-L1脂肪细胞和264.7巨噬细胞后发现，未与RAW264.7巨噬细胞共培养的3T3-L1脂肪细胞相比，脂联素的分泌明显增肌。
研究结果表明，GLP-1诱导向M2型巨噬细胞极化，M2型巨噬细胞极化可能有助于帮助GLP-1抵抗和心血管疾病。在这项研究中GLP-1活化巨噬细胞的功效主要于诱导STAT3的激活有关。GLP-1诱导巨噬细胞分化走向M2型，导致脂肪细胞脂联素分泌增加。（：）
Glucagon-like peptide-1 (GLP-1) induces M2 polarization of human macrophages via STAT3 activation
Daisuke Shiraishia,Yukio Fujiwara,et al.
It is known that glucagon-like peptide-1 (GLP-1) is a hormone secreted postprandially from the L-cells of the small intestine and regulates glucose homeostasis. GLP-1 is now used for the treatment of diabetes because of its beneficial role against insulin resistance. The GLP-1 receptor (GLP-1R) is expressed on many cell types, including macrophages, and GLP-1 suppresses the development of atherosclerosis by inhibiting macrophage function. However, there have so far been few studies that have investigated the significance of GLP-1/GLP-1R signaling in macrophage activation. In the present study, we examined the effect of GLP-1 and exenatide, a GLP-1R agonist, on human monocyte-derived macrophage (HMDM) activation. We found that GLP-1 induced signal transducer and activator of transcription 3 (STAT3) activation. Silencing of GLP-1R suppressed the GLP-1-induced STAT3 activation. In addition, alternatively activated (M2) macrophage-related molecules, such as IL-1, CD163, and CD24 in HMDM, were significantly upregulated by GLP-Furthermore, the co-culture of 3T3-L1 adipocytes with GLP-1-treated RAW 264.7 macrophages increased the secretion of adiponectin compared to co-culture of the 3T3-L1 adipocytes with untreated RAW 264.7 macrophages. Our results demonstrate that GLP-1 induces macrophage polarization toward the M2 , which may contribute to the protective effects of GLP-1 against diabetes and cardiovascular diseases. We examined the effect of GLP-1 on macrophage activation in this study. GLP-1 induces STAT3 activation in human macrophages. GLP-1 induces macrophages differentiation toward the M2 . GLP-1-treated macrophages increase adiponectin secretion from adipocytes.
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