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富含共轭亚油酸的油未能减轻雄性 CD2F1 小鼠结肠-26 肿瘤诱导的晚期癌症恶病质的消耗。

c9t11-Conjugated linoleic acid-rich oil fails to attenuate wasting in colon-26 tumor-induced late-stage cancer cachexia in male CD2F1 mice.

机构信息

Department of Human Nutrition, College of Education and Human Ecology, The Ohio State University, Columbus, OH 43210, USA.

出版信息

Mol Nutr Food Res. 2011 Feb;55(2):268-77. doi: 10.1002/mnfr.201000176. Epub 2010 Sep 8.

Abstract

SCOPE

Cancer cachexia is characterized by muscle and adipose tissue wasting caused partly by chronic, systemic inflammation. Conjugated linoleic acids (CLAs) are a group of fatty acids with various properties including anti-inflammatory cis9, trans11 (c9t11)-CLA and lipid-mobilizing trans10, cis12 (t10c12)-CLA. The purpose of this study was to test whether dietary supplementation of a c9t11-CLA-rich oil (6:1 c9t11:t10c12) could attenuate wasting of muscle and adipose tissue in colon-26 adenocarcinoma-induced cachexia in mice.

METHODS AND RESULTS

Loss of body weight, muscle and adipose tissue mass caused by tumors were not rescued by supplementation with the c9t11-CLA-rich oil. In quadriceps muscle, c9t11-CLA-rich oil exacerbated tumor-induced gene expression of inflammatory markers tumor necrosis factor-α, IL-6 receptor and the E3 ligase MuRF-1 involved in muscle proteolysis. In epididymal adipose tissue, tumor-driven delipidation and atrophy was aggravated by the c9,t11-CLA-rich oil, demonstrated by further reduced adipocyte size and lower adiponectin expression. However, expression of inflammatory cytokines and macrophage markers were not altered by tumors, or CLA supplementation.

CONCLUSION

These data suggest that addition of c9t11-CLA-rich oil (0.6% c9t11, 0.1% t10c12) in diet did not ameliorate wasting in mice with cancer cachexia. Instead, it increased expression of inflammatory markers in the muscle and increased adipose delipidation.

摘要

研究范围

癌症恶病质的特征是肌肉和脂肪组织消耗,部分原因是慢性系统性炎症。共轭亚油酸(CLA)是一组具有不同特性的脂肪酸,包括具有抗炎作用的顺式 9,反式 11(c9t11)-CLA 和脂解作用的反式 10,顺式 12(t10c12)-CLA。本研究旨在测试富含 c9t11-CLA 的油(6:1 c9t11:t10c12)的饮食补充是否可以减轻结肠 26 腺癌诱导的恶病质小鼠的肌肉和脂肪组织消耗。

方法和结果

富含 c9t11-CLA 的油补充并不能挽救肿瘤引起的体重、肌肉和脂肪组织损失。在股四头肌中,富含 c9t11-CLA 的油加剧了肿瘤诱导的炎症标志物肿瘤坏死因子-α、IL-6 受体和参与肌肉蛋白水解的 E3 连接酶 MuRF-1 的基因表达。在附睾脂肪组织中,肿瘤驱动的脱脂和萎缩被富含 c9t11-CLA 的油加剧,表现为脂肪细胞大小进一步减小和脂联素表达降低。然而,肿瘤或 CLA 补充并未改变炎症细胞因子和巨噬细胞标志物的表达。

结论

这些数据表明,富含 c9t11-CLA 的油(0.6% c9t11,0.1% t10c12)在饮食中的添加并未改善癌症恶病质小鼠的消耗。相反,它增加了肌肉中炎症标志物的表达并增加了脂肪的脱脂。

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