Genetic vulnerability to diet-induced obesity in the C57BL/6J mouse: physiological and molecular characteristics.
The development of the metabolic syndrome in an increasing percentage of the populations of Western societies, particularly in the United States, requires valid models for establishing basic biochemical changes and performing preclinical studies on potential drug targets. The C57BL/6J mouse has become an important model for understanding the interplay between genetic background and environmental challenges such as high-fat/high-calorie diets that predispose to the development of the metabolic syndrome. This review highlights metabolic and signal transduction features that are altered during the course of disease progression, many of which mirror the human situation.
Collins
Sheila
S
Department of Pharmacology, Duke University Medical Center, Durham, NC 27710, USA. colli008@mc.duke.edu
Martin
Tonya L
TL
Surwit
Richard S
RS
Robidoux
Jacques
J
D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D002395:Catecholamines / Q000378:metabolism; D004032:Diet / Q000009:adverse effects*; D020022:Genetic Predisposition to Disease; D051379:Mice; D008810:Mice, Inbred C57BL / Q000235:genetics* / Q000378:metabolism; D009765:Obesity / Q000209:etiology* / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology; D015398:Signal Transduction / Q000502:physiology
D002395:Catecholamines