Mesenchymal stem cells (MSCs) can be obtained from almost all tissues and present promising therapeutic effects for metabolic diseases. Human adipose-derived MSCs (hASCs) have recently been widely studied due to their easy access and low immunity. Thus, we intended to figure out the effects and potential mechanism of hASCs on obesity in high-fat-diet (HFD)-induced obese mice. Following 16 weeks of being fed HFD, hASCs were intravenously injected. Two weeks later, body weight, body composition, and energy expenditure were evaluated. Additionally, the phenotypes of macrophages infiltrating adipose tissue were analyzed. The results revealed that hASCs administration significantly reduced adipose tissue weight, adipocyte size, and fat mass and exerted beneficial effects in serum lipid profile. This anti-obesity effect was mediated by the increased O 2 consumption, CO 2 production, and energy expenditure, which was further evidenced by the upregulation of uncoupling protein-1 (UCP-1) and metabolism-associated genes. Furthermore, hASCs infusion increased the amount of alternatively activated (M2) macrophages in adipose tissue, and the expression of pro-inflammatory cytokines-related genes was reduced. Taken together, these results indicated that hASCs suppressed obesity by increasing UCP-1 expression and enhancing energy expenditure, and this effect might be due to the increased M2 macrophages.

中文翻译：

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间充质干细胞对肥胖小鼠的抗肥胖作用及机制

间充质干细胞 (MSCs) 几乎可以从所有组织中获得，对代谢疾病具有良好的治疗效果。人类脂肪来源的间充质干细胞 (hASCs) 由于其易于获取和低免疫力而最近被广泛研究。因此，我们打算找出 hASCs 对高脂饮食 (HFD) 诱导的肥胖小鼠肥胖的影响和潜在机制。在喂食 HFD 16 周后，静脉注射 hASC。两周后，评估体重、身体成分和能量消耗。此外，还分析了浸润脂肪组织的巨噬细胞的表型。结果表明，hASCs 给药显着降低了脂肪组织重量、脂肪细胞大小和脂肪量，并对血清脂质谱产生了有益影响。这种抗肥胖作用是由增加的 O 2 消耗、CO 2 产生和能量消耗介导的，解偶联蛋白 1 (UCP-1) 和代谢相关基因的上调进一步证明了这一点。此外，hASCs 输注增加了脂肪组织中交替激活 (M2) 巨噬细胞的数量，并降低了促炎细胞因子相关基因的表达。总之，这些结果表明 hASCs 通过增加 UCP-1 表达和增强能量消耗来抑制肥胖，这种效果可能是由于 M2 巨噬细胞的增加。hASCs 输注增加了脂肪组织中交替激活 (M2) 巨噬细胞的数量，并降低了促炎细胞因子相关基因的表达。总之，这些结果表明 hASCs 通过增加 UCP-1 表达和增强能量消耗来抑制肥胖，这种效果可能是由于 M2 巨噬细胞的增加。hASCs 输注增加了脂肪组织中交替激活 (M2) 巨噬细胞的数量，并降低了促炎细胞因子相关基因的表达。总之，这些结果表明 hASCs 通过增加 UCP-1 表达和增强能量消耗来抑制肥胖，这种效果可能是由于 M2 巨噬细胞的增加。