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本文引用的文献

1
Age and energy intake interact to modify cell stress pathways and stroke outcome.年龄和能量摄入相互作用,改变细胞应激途径和中风结果。
Ann Neurol. 2010 Jan;67(1):41-52. doi: 10.1002/ana.21798.
2
Prevalence and trends in obesity among US adults, 1999-2008.美国成年人肥胖率的流行趋势及变化,1999-2008 年。
JAMA. 2010 Jan 20;303(3):235-41. doi: 10.1001/jama.2009.2014. Epub 2010 Jan 13.
3
Genetic variation in the murine lifespan response to dietary restriction: from life extension to life shortening.限制饮食对小鼠寿命反应的遗传变异:从延长寿命到缩短寿命。
Aging Cell. 2010 Feb;9(1):92-5. doi: 10.1111/j.1474-9726.2009.00533.x. Epub 2009 Oct 30.
4
Mechanisms of obesity and related pathology: linking immune responses to metabolic stress.肥胖及其相关病理机制:将免疫反应与代谢应激联系起来。
FEBS J. 2009 Oct;276(20):5747-54. doi: 10.1111/j.1742-4658.2009.07304.x. Epub 2009 Sep 15.
5
Physical exercise improves motor and short-term social memory deficits in reserpinized rats.体育锻炼可改善利血平化大鼠的运动和短期社交记忆缺陷。
Brain Res Bull. 2009 Aug 14;79(6):452-7. doi: 10.1016/j.brainresbull.2009.05.005. Epub 2009 May 20.
6
Exercise and the brain: something to chew on.运动与大脑:值得思考的问题。
Trends Neurosci. 2009 May;32(5):283-90. doi: 10.1016/j.tins.2008.12.007. Epub 2009 Apr 6.
7
Voluntary exercise and caloric restriction enhance hippocampal dendritic spine density and BDNF levels in diabetic mice.自愿运动和热量限制可提高糖尿病小鼠海马体树突棘密度和脑源性神经营养因子水平。
Hippocampus. 2009 Oct;19(10):951-61. doi: 10.1002/hipo.20577.
8
Caloric restriction-induced life extension of rats and mice: a critique of proposed mechanisms.热量限制诱导大鼠和小鼠寿命延长:对所提出机制的批判
Biochim Biophys Acta. 2009 Oct;1790(10):1040-8. doi: 10.1016/j.bbagen.2009.02.011. Epub 2009 Feb 27.
9
Novel mechanism for obesity-induced colon cancer progression.肥胖诱导结肠癌进展的新机制。
Carcinogenesis. 2009 Apr;30(4):690-7. doi: 10.1093/carcin/bgp041. Epub 2009 Feb 12.
10
Restorative effect of endurance exercise on behavioral deficits in the chronic mouse model of Parkinson's disease with severe neurodegeneration.耐力运动对严重神经退行性变的帕金森病慢性小鼠模型行为缺陷的恢复作用。
BMC Neurosci. 2009 Jan 20;10:6. doi: 10.1186/1471-2202-10-6.

“对照”实验动物代谢病态化:为何这很重要。

"Control" laboratory rodents are metabolically morbid: why it matters.

机构信息

Metabolism Unit, Laboratory of Clinical Investigation, Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA.

出版信息

Proc Natl Acad Sci U S A. 2010 Apr 6;107(14):6127-33. doi: 10.1073/pnas.0912955107. Epub 2010 Mar 1.

DOI:10.1073/pnas.0912955107
PMID:20194732
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2852022/
Abstract

Failure to recognize that many standard control rats and mice used in biomedical research are sedentary, obese, glucose intolerant, and on a trajectory to premature death may confound data interpretation and outcomes of human studies. Fundamental aspects of cellular physiology, vulnerability to oxidative stress, inflammation, and associated diseases are among the many biological processes affected by dietary energy intake and exercise. Although overfed sedentary rodents may be reasonable models for the study of obesity in humans, treatments shown to be efficacious in these animal models may prove ineffective or exhibit novel side effects in active, normal-weight subjects.

摘要

未能认识到,许多在生物医学研究中使用的标准的对照大鼠和小鼠都是久坐不动、肥胖、葡萄糖不耐受,并处于过早死亡的轨迹上,这可能会混淆数据解释和人类研究的结果。细胞生理学的基本方面、对氧化应激、炎症和相关疾病的易感性是受饮食能量摄入和运动影响的众多生物学过程之一。虽然过度喂养的久坐不动的啮齿动物可能是研究人类肥胖的合理模型,但在这些动物模型中显示有效的治疗方法在活跃的、正常体重的受试者中可能无效或表现出新的副作用。