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基础代谢率对癌症的影响:一项孟德尔随机化研究

Effect of Basal Metabolic Rate on Cancer: A Mendelian Randomization Study.

作者信息

Ng Jack C M, Schooling C Mary

机构信息

School of Public Health, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region, China.

Department of Environmental, Occupational, and Geospatial Health Sciences, Graduate School of Public Health and Health Policy, The City University of New York, New York, NY, United States.

出版信息

Front Genet. 2021 Sep 9;12:735541. doi: 10.3389/fgene.2021.735541. eCollection 2021.

Abstract

Basal metabolic rate is associated with cancer, but these observations are open to confounding. Limited evidence from Mendelian randomization studies exists, with inconclusive results. Moreover, whether basal metabolic rate has a similar role in cancer for men and women independent of insulin-like growth factor 1 increasing cancer risk has not been investigated. We conducted a two-sample Mendelian randomization study using summary data from the UK Biobank to estimate the causal effect of basal metabolic rate on cancer. Overall and sex-specific analysis and multiple sensitivity analyses were performed including multivariable Mendelian randomization to control for insulin-like growth factor 1. We obtained 782 genetic variants strongly (-value < 5 × 10) and independently ( < 0.01) predicting basal metabolic rate. Genetically predicted higher basal metabolic rate was associated with an increase in cancer risk overall (odds ratio, 1.06; 95% confidence interval, 1.02-1.10) with similar estimates by sex (odds ratio for men, 1.07; 95% confidence interval, 1.002-1.14; odds ratio for women, 1.06; 95% confidence interval, 0.995-1.12). Sensitivity analyses including adjustment for insulin-like growth factor 1 showed directionally consistent results. Higher basal metabolic rate might increase cancer risk. Basal metabolic rate as a potential modifiable target of cancer prevention warrants further study.

摘要

基础代谢率与癌症有关,但这些观察结果容易受到混杂因素的影响。孟德尔随机化研究的证据有限,结果尚无定论。此外,基础代谢率在男性和女性癌症中是否具有类似作用,且独立于胰岛素样生长因子1增加癌症风险这一点尚未得到研究。我们使用英国生物银行的汇总数据进行了一项两样本孟德尔随机化研究,以估计基础代谢率对癌症的因果效应。进行了总体和性别特异性分析以及多项敏感性分析,包括多变量孟德尔随机化以控制胰岛素样生长因子1。我们获得了782个强烈(-值<5×10)且独立(<0.01)预测基础代谢率的基因变异。遗传预测的较高基础代谢率与总体癌症风险增加相关(优势比,1.06;95%置信区间,1.02 - 1.10),按性别估计相似(男性优势比,1.07;95%置信区间,1.002 - 1.14;女性优势比,1.06;95%置信区间,0.995 - 1.12)。包括对胰岛素样生长因子1进行调整的敏感性分析显示结果方向一致。较高的基础代谢率可能会增加癌症风险。基础代谢率作为癌症预防的一个潜在可改变靶点值得进一步研究。

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