Abstract
Maternal obesity affects the incidence of cardiovascular disease and diabetes in offspring. Also the use of assisted reproductive technologies (ART) has been associated with cardiovascular deficiencies in offspring. Obese women often suffer from infertility and use ART to achieve a pregnancy, but the combined effects of maternal obesity and ART on cardiovascular health and incidence of diabetes in the offspring is not known. Here, we report the effects of the use of ART within an obesogenic environment, consisting of feeding a western diet (WD) to dams and offspring, on resistance artery function and presence of diabetes biomarkers in juvenile mice offspring. Our results indicate that WD and ART interacted to induce endothelial dysfunction in mesenteric resistance arteries isolated from 7-week-old mice offspring. This was determined by presence of a reduced acetylcholine-induced dilation compared to controls. The arteries from these WD-ART mice also had greater wall cross-sectional areas and wall to lumen ratios indicative of vascular hypertrophic remodeling. Of the diabetes biomarkers measured, only resistin was affected by a WD×ART interaction. Serum resistin was significantly greater in WD-ART offspring compared to controls. Diet and sex effects were observed in other diabetes biomarkers. Our conclusion is that in mice the use of ART within an obesogenic environment interacts to favor the development of endothelial dysfunction in the resistance arteries of juvenile offspring, while having marginal effects on diabetes biomarkers.
Highlights
Obesity has become a major health problem worldwide [1,2]
No significant differences were observed between arteries from males or females on the constriction caused by KCl-induced depolarization (Figure 2B)
The primary finding of the present study is that the use of assisted reproductive technologies (ART) in an obesogenic environment is associated with a reduced acetylcholine-induce dilation of mesenteric resistance arteries in juvenile mice offspring
Summary
Obesity has become a major health problem worldwide [1,2]. Excessive body weight in the form of accumulated adipose tissue is accompanied by adverse pathophysiological conditions. The epidemic proportions at which obesity is increasing are associated with an increased consumption of hypercaloric diets rich in fats and carbohydrates, as well as with more sedentary lifestyles [3,4,5]. In addition to these factors, evidence is increasing that indicates exposure to an obesogenic environment during embryonic and fetal development programs individuals for obesity, hypertension and T2DM later in life [6,7,8,9,10,11,12,13]. This developmental programming of adult diseases is hypothesized to participate in perpetuating the incidence of obesity and cardiovascular disease across generations [5]
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