Developmental programming resulting from maternal obesity in mice: effects on myocardial ischaemia-reperfusion injury.
A comprehensive number of epidemiological and animal studies suggest that prenatal and early life events are important determinants for disorders later in life. Among them, prenatal stress (i.e. stress experienced by the pregnant mother with impact on the fetal ontogeny) has clear programming effects on the cardiovascular system. A fetus developing in adverse conditions becomes an adult who is susceptible to disease, which may include hypertension, insulin resistance, altered blood lipid levels and cardiovascular disease. Recent evidence demonstrates that maternal programming can occur in the absence of other adverse environmental factors. Obesity, which is becoming a problem of large proportions in Western countries, is a possible cause of programming. With over 30% of the population of the USA currently obese, many mothers suffer from obesity during their child-bearing years (in fact, these conditions are often aggravated during pregnancy). One of the targets of programming is the cardiovascular system, and reported consequences include hypertension, endothelial dysfunction and vascular abnormalities. The overall goal of our study was to investigate the susceptibility of the heart to ischaemia-reperfusion in an animal model of maternal obesity. Our data demonstrate that normal (non-mutant) offspring from obese agouti mouse dams had an increased susceptibility to ischaemia-reperfusion injury. These data may provide insights into the long-term cardiovascular consequences of programming.
Calvert
John W
JW
Department of Surgery, Division of Cardiothoracic Surgery, Emory University School of Medicine, Atlanta, GA, USA.
Lefer
David J
DJ
Gundewar
Susheel
S
Poston
Lucilla
L
Coetzee
William A
WA
D000818:Animals; D004195:Disease Models, Animal; D004452:Echocardiography; D005260:Female; D008297:Male; D051379:Mice; D015428:Myocardial Reperfusion Injury / Q000209:etiology* / Q000473:pathology; D009765:Obesity / Q000503:physiopathology*; D011247:Pregnancy; D011248:Pregnancy Complications / Q000503:physiopathology; D011297:Prenatal Exposure Delayed Effects; D039401:Prenatal Nutritional Physiological Phenomena; D012737:Sex Factors; D016277:Ventricular Function, Left / Q000502:physiology