"Control" laboratory rodents are metabolically morbid: Why it matters

被引:274
作者
Martin, Bronwen [2 ]
Ji, Sunggoan [2 ]
Maudsley, Stuart [3 ]
Mattson, Mark P. [1 ]
机构
[1] NIA, Cellular & Mol Neurosci Sect, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA
[2] NIA, Metab Unit, Clin Invest Lab, Intramural Res Program, Baltimore, MD 21224 USA
[3] NIA, Receptor Pharmacol Unit, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA
基金
美国国家卫生研究院;
关键词
cancer; clinical trials; exercise; insulin resistance; obesity; 11-BETA-HYDROXYSTEROID DEHYDROGENASE TYPE-1; CHRONIC CALORIC RESTRICTION; DIETARY ENERGY RESTRICTION; TRANSGENIC MOUSE MODEL; INSULIN-RESISTANCE; FOOD RESTRICTION; BODY-WEIGHT; BEHAVIORAL DEFICITS; ENDURANCE EXERCISE; VOLUNTARY EXERCISE;
D O I
10.1073/pnas.0912955107
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
收藏
页码:6127 / 6133
页数:7
相关论文
共 105 条
[41]   EFFECT OF EXERCISE TRAINING ON WHOLE-BODY INSULIN SENSITIVITY AND RESPONSIVENESS [J].
JAMES, DE ;
KRAEGEN, EW ;
CHISHOLM, DJ .
JOURNAL OF APPLIED PHYSIOLOGY, 1984, 56 (05) :1217-1222
[42]   Inflammation as Therapeutic Objective in Stroke [J].
Jordan, Joaquin ;
Segura, Tomas ;
Brea, David ;
Galindo, Maria F. ;
Castillo, Jose .
CURRENT PHARMACEUTICAL DESIGN, 2008, 14 (33) :3549-3564
[43]   Mechanisms of obesity and related pathology: linking immune responses to metabolic stress [J].
Karalis, Katia P. ;
Giannogonas, Panagiotis ;
Kodela, Elisavet ;
Koutmani, Yassemi ;
Zoumakis, Manolis ;
Teli, Thalia .
FEBS JOURNAL, 2009, 276 (20) :5747-5754
[44]   Osteopontin expression in human and murine obesity: Extensive local up-regulation in adipose tissue but minimal systemic alterations [J].
Kiefer, Florian W. ;
Zeyda, Maximilian ;
Todoric, Jelena ;
Huber, Joakim ;
Geyeregger, Rene ;
Weichhart, Thomas ;
Aszmann, Oskar ;
Ludvik, Bernhard ;
Silberhumer, Gerd R. ;
Prager, Gerhard ;
Stulnig, Thomas M. .
ENDOCRINOLOGY, 2008, 149 (03) :1350-1357
[45]   Environmental enrichment reduces Aβ levels and amyloid deposition in transgenic mice [J].
Lazarov, O ;
Robinson, J ;
Tang, YP ;
Hairston, IS ;
Korade-Mirnics, Z ;
Lee, VMY ;
Hersh, LB ;
Sapolsky, RM ;
Mirnics, K ;
Sisodia, SS .
CELL, 2005, 120 (05) :701-713
[46]   Randomized phase II designs in cancer clinical trials: Current status and future directions [J].
Lee, JJ ;
Feng, L .
JOURNAL OF CLINICAL ONCOLOGY, 2005, 23 (19) :4450-4457
[47]   Genetic variation in the murine lifespan response to dietary restriction: from life extension to life shortening [J].
Liao, Chen-Yu ;
Rikke, Brad A. ;
Johnson, Thomas E. ;
Diaz, Vivian ;
Nelson, James F. .
AGING CELL, 2010, 9 (01) :92-95
[48]   The curry spice curcumin reduces oxidative damage and amyloid pathology in an Alzheimer transgenic mouse [J].
Lim, GP ;
Chu, T ;
Yang, FS ;
Beech, W ;
Frautschy, SA ;
Cole, GM .
JOURNAL OF NEUROSCIENCE, 2001, 21 (21) :8370-8377
[49]   Effects of TNF-α neutralization on adipocytokines and skeletal muscle adiposity in the metabolic syndrome [J].
Lo, Janet ;
Bernstein, L. Elizabeth ;
Canavan, Bridget ;
Torriani, Martin ;
Jackson, Malaka B. ;
Ahima, Rexford S. ;
Grinspoon, Steven K. .
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2007, 293 (01) :E102-E109
[50]  
Lodder J, 2000, NEUROSCI RES COMMUN, V26, P173, DOI 10.1002/1520-6769(200005/06)26:3<173::AID-NRC5>3.3.CO