P1-41 Developmental programming of cardiovascular dysfunction by maternal obesity

2007 ◽  
Vol 83 ◽  
pp. S94
Author(s):  
A.M. Samuelsson ◽  
A.I. Awopetu ◽  
P.A. Matthews ◽  
P.D. Taylor ◽  
L. Poston
2014 ◽  
Vol 2014 ◽  
pp. 1-14 ◽  
Author(s):  
Stephanie A. Segovia ◽  
Mark H. Vickers ◽  
Clint Gray ◽  
Clare M. Reynolds

The prevalence of obesity, especially in women of child-bearing age, is a global health concern. In addition to increasing the immediate risk of gestational complications, there is accumulating evidence that maternal obesity also has long-term consequences for the offspring. The concept of developmental programming describes the process in which an environmental stimulus, including altered nutrition, during critical periods of development can program alterations in organogenesis, tissue development, and metabolism, predisposing offspring to obesity and metabolic and cardiovascular disorders in later life. Although the mechanisms underpinning programming of metabolic disorders remain poorly defined, it has become increasingly clear that low-grade inflammation is associated with obesity and its comorbidities. This review will discuss maternal metainflammation as a mediator of programming in insulin sensitive tissues in offspring. Use of nutritional anti-inflammatories in pregnancy including omega 3 fatty acids, resveratrol, curcumin, and taurine may provide beneficial intervention strategies to ameliorate maternal obesity-induced programming.


2019 ◽  
Vol 11 (3) ◽  
pp. 297-306 ◽  
Author(s):  
Hillary F. Huber ◽  
Susan L. Jenkins ◽  
Cun Li ◽  
Peter W. Nathanielsz

AbstractNonhuman primate (NHP) studies are crucial to biomedical research. NHPs are the species most similar to humans in lifespan, body size, and hormonal profiles. Planning research requires statistical power evaluation, which is difficult to perform when lacking directly relevant preliminary data. This is especially true for NHP developmental programming studies, which are scarce. We review the sample sizes reported, challenges, areas needing further work, and goals of NHP maternal nutritional programming studies. The literature search included 27 keywords, for example, maternal obesity, intrauterine growth restriction, maternal high-fat diet, and maternal nutrient reduction. Only fetal and postnatal offspring studies involving tissue collection or imaging were included. Twenty-eight studies investigated maternal over-nutrition and 33 under-nutrition; 23 involved macaques and 38 baboons. Analysis by sex was performed in 19; minimum group size ranged from 1 to 8 (mean 4.7 ± 0.52, median 4, mode 3) and maximum group size from 3 to 16 (8.3 ± 0.93, 8, 8). Sexes were pooled in 42 studies; minimum group size ranged from 2 to 16 (mean 5.3 ± 0.35, median 6, mode 6) and maximum group size from 4 to 26 (10.2 ± 0.92, 8, 8). A typical study with sex-based analyses had group size minimum 4 and maximum 8 per sex. Among studies with sexes pooled, minimum group size averaged 6 and maximum 8. All studies reported some significant differences between groups. Therefore, studies with group sizes 3–8 can detect significance between groups. To address deficiencies in the literature, goals include increasing age range, more frequently considering sex as a biological variable, expanding topics, replicating studies, exploring intergenerational effects, and examining interventions.


Author(s):  
Paul D. Taylor ◽  
Phillippa A. Matthews ◽  
Imran Y. Khan ◽  
Douglas Rees ◽  
Nozomi Itani ◽  
...  

2007 ◽  
Vol 83 ◽  
pp. S72
Author(s):  
A.M. Samuelsson ◽  
P.A. Matthews ◽  
P.D. Taylor ◽  
L. Poston

2014 ◽  
Vol 210 (3) ◽  
pp. 508-523 ◽  
Author(s):  
P. D. Taylor ◽  
A.-M. Samuelsson ◽  
L. Poston

2019 ◽  
Vol 17 (2) ◽  
pp. 147-152 ◽  
Author(s):  
Zewen Chen ◽  
Lei Wang ◽  
Jun Ke ◽  
Daliao Xiao

Background: Epidemiological studies and experimental studies have demonstrated that intrauterine adverse environment increases the risk of Cardiovascular Disease (CVD) in adulthood. However, whether an individual develops a cardiovascular dysfunctional phenotype may depend on genetic background, age, and sex. </P><P> Methods: In this review, we summarize some of the recent experimental animal studies in the developmental programming of adult CVD with an emphasis on sex differences and the potential role of estrogen in mediating sexual dimorphism. </P><P> Results: Few epidemiological studies report the effect of sex on the developmental programming of CVD. However, numerous experimental animal studies have shown a sex difference in fetal programming of adult cardiovascular dysfunction. Most of the animal studies indicate that male offspring develop cardiovascular dysfunction and CVD in adulthood, whereas adult females appear to be protected. Estrogen is one of the key factors that contributes to the sex difference of adult CVD. Estrogen/its Receptor (ER) may interact with the RAS system by changes of DNA methylation patterns at the target gene promoter, serve as an antioxidant to counteract the prenatal insults-induced heightened ROS, and function as an eNOS activator to increase vasodilation, resulting in the protection of female offspring from the development of hypertension and other CVDs. </P><P> Conclusion: These studies suggest that estrogen/ER may contribute to sex differences in cardiovascular response to an adverse intrauterine environment and play a significant role in modulating the cardiovascular response in adulthood.


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