Suppr超能文献

脂肪组织特异性单核细胞趋化蛋白-1缺乏可减少小鼠Lewis肺癌的肺转移。

Adipose-specific Monocyte Chemotactic Protein-1 Deficiency Reduces Pulmonary Metastasis of Lewis Lung Carcinoma in Mice.

作者信息

Sundaram Sneha, Yan Lin

机构信息

U.S. Department of Agriculture, Agricultural Research Service, Grand Forks Human Nutrition Research Center, Grand Forks, ND, U.S.A.

出版信息

Anticancer Res. 2019 Apr;39(4):1729-1738. doi: 10.21873/anticanres.13279.

Abstract

AIM

Monocyte chemotactic protein-1 (MCP1) is a potent adipokine. This study tested the hypothesis that adipose-produced MCP1 contributes to metastasis.

MATERIALS AND METHODS

In a spontaneous metastasis model of Lewis lung carcinoma (LLC), male adipose MCP1-deficient (Mcp1) and wild-type (WT) mice were fed the AIN93G diet or a high-fat diet (HFD) for 11 weeks. Lung metastasis from a subcutaneous tumor was the primary endpoint.

RESULTS

The adipose expression of MCP1 was lower in Mcp1 mice than in WT controls. The HFD increased the number of lung metastases in WT mice. The number of metastasis was significantly lower in the HFD-fed Mcp1 mice than in the HFD-fed WT mice. Compared to the WT mice, adipose MCP1 deficiency lowered plasma concentrations of insulin, proinflammatory adipokines (leptin, plasminogen activator inhibitor-1, and resistin), and angiogenic markers (vascular endothelial growth factor, hepatocyte growth factor, and angiopoietin-2).

CONCLUSION

Adipose MCP1 deficiency attenuates HFD-enhanced pulmonary metastasis of LLC.

摘要

目的

单核细胞趋化蛋白-1(MCP1)是一种强效脂肪因子。本研究检验了脂肪组织产生的MCP1促进转移这一假说。

材料与方法

在Lewis肺癌(LLC)自发转移模型中,给雄性脂肪组织MCP1缺陷(Mcp1)小鼠和野生型(WT)小鼠喂食AIN93G饮食或高脂饮食(HFD)11周。皮下肿瘤的肺转移是主要终点。

结果

Mcp1小鼠脂肪组织中MCP1的表达低于WT对照。高脂饮食增加了WT小鼠的肺转移数量。喂食高脂饮食的Mcp1小鼠的转移数量显著低于喂食高脂饮食的WT小鼠。与WT小鼠相比,脂肪组织MCP1缺陷降低了血浆中胰岛素、促炎脂肪因子(瘦素、纤溶酶原激活物抑制剂-1和抵抗素)以及血管生成标志物(血管内皮生长因子、肝细胞生长因子和血管生成素-2)的浓度。

结论

脂肪组织MCP1缺陷减弱了高脂饮食增强的LLC肺转移。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验