據了解，胰高血糖素樣肽1（GLP-1）是餐後從小腸L型細胞分泌的一種具有調節葡萄糖穩態功能的激素。
目前，GLP-1已被用於糖尿病的治療，主要原因是其對胰島素抵抗具有有益作用。許多類型的細胞包括巨噬細胞都表達GLP-1受體（GLP-1R），GLP-1通過抑制巨噬細胞功能，進而抑制動脈粥樣硬化的發展。
然而，迄今為止有關GLP-1/GLP-1R信號在巨噬細胞活化中的作用相關研究很少。在一項最新研究中，科研人員探討了GLP-1和艾塞那肽(Exenatide) 對人單核細胞源性巨噬細胞（HMDM）激活的作用，艾塞那肽是GLP-1R激動劑，是首個化學全合成的腸促胰島素類似物，可降低2型糖尿病患者的空腹和餐後血糖。
研究發現，GLP-1誘導轉錄因子3（STAT3）活化激活的信號轉導。GLP-1R沉默後能抑制GLP-1誘導的STAT3活化。此外，激活型（M2）巨噬細胞相關的分子如IL-1、CD163等在接受GLP刺激後都顯著上調。
此外， GLP-1處理共培養的RAW3T3-L1脂肪細胞和264.7巨噬細胞後發現，未與RAW264.7巨噬細胞共培養的3T3-L1脂肪細胞相比，脂聯素的分泌明顯增肌。
研究結果表明，GLP-1誘導向M2型巨噬細胞極化，M2型巨噬細胞極化可能有助於幫助GLP-1抵抗糖尿病和心血管疾病。在這項研究中GLP-1活化巨噬細胞的功效主要於誘導STAT3的激活有關。GLP-1誘導巨噬細胞分化走向M2型，導致脂肪細胞脂聯素分泌增加。（生物谷：Bioon.com）
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 phenotype, 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 phenotype. GLP-1-treated macrophages increase adiponectin secretion from adipocytes.