scholarly journals N-acetylcysteine protects neonatal mice from ventricular hypertrophy induced by maternal obesity in a sex-specific manner

2021 ◽  
Vol 133 ◽  
pp. 110989
Author(s):  
Jialing Zhang ◽  
Li Cao ◽  
Yanfeng Tan ◽  
Yuanzheng Zheng ◽  
Yonghao Gui
Keyword(s):  
Ventricular Hypertrophy ◽  
Maternal Obesity ◽  
Neonatal Mice ◽  
Specific Manner

scholarly journals Maternal obesity reprograms offspring's executive brain centers in a sex-specific manner?

2018 ◽  
Vol 145 (5) ◽  
pp. 358-361 ◽  
Author(s):  
Kaja Plucińska ◽  
Steven W. Barger
Keyword(s):  
Maternal Obesity ◽  
Specific Manner

scholarly journals NFATc3 is required for chronic hypoxia-induced pulmonary hypertension in adult and neonatal mice

2011 ◽  
Vol 301 (6) ◽  
pp. L872-L880 ◽  
Author(s):  
R. Bierer ◽  
C. H. Nitta ◽  
J. Friedman ◽  
S. Codianni ◽  
S. de Frutos ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Vascular Remodeling ◽  
Ventricular Hypertrophy ◽  
Chronic Hypoxia ◽  
Systolic Pressure ◽  
Right Ventricular Systolic Pressure ◽  
Ventricular Systolic Pressure ◽  
Neonatal Mice ◽  
Adult Mice

Pulmonary hypertension occurs with prolonged exposure to chronic hypoxia in both adults and neonates. The Ca2+-dependent transcription factor, nuclear factor of activated T cells isoform c3 (NFATc3), has been implicated in chronic hypoxia-induced pulmonary arterial remodeling in adult mice. Therefore, we hypothesized that NFATc3 is required for chronic hypoxia-induced pulmonary hypertension in adult and neonatal mice. The aim of this study was to determine whether 1) NFATc3 mediates chronic hypoxia-induced increases in right ventricular systolic pressure in adult mice; 2) NFATc3 is activated in neonatal mice exposed to chronic hypoxia; and 3) NFATc3 is involved in chronic hypoxia-induced right ventricular hypertrophy and pulmonary vascular remodeling in neonatal mice. Adult mice were exposed to hypobaric hypoxia for 2, 7, and 21 days. Neonatal mouse pups were exposed for 7 days to hypobaric chronic hypoxia within 2 days after delivery. Hypoxia-induced increases in right ventricular systolic pressure were absent in NFATc3 knockout adult mice. In neonatal mice, chronic hypoxia caused NFAT activation in whole lung and nuclear accumulation of NFATc3 in both pulmonary vascular smooth muscle and endothelial cells. In addition, heterozygous NFATc3 neonates showed less right ventricular hypertrophy and pulmonary artery wall thickness in response to chronic hypoxia than did wild-type neonates. Our results suggest that NFATc3 mediates pulmonary hypertension and vascular remodeling in both adult and neonatal mice.

scholarly journals Choline Supplementation in Obese Mouse Dams Alters Offspring DNA Methylation in a Time-Specific Manner

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 763-763
Author(s):  
Xinyin Jiang ◽  
Hunter Korsmo ◽  
Moshe Dembitzer ◽  
Sarah Khaldi ◽  
Shameera Sheeraz
Keyword(s):  
Dna Methylation ◽  
Adipose Tissue ◽  
Maternal Obesity ◽  
Fetal Liver ◽  
Obese Mouse ◽  
Global Dna Methylation ◽  
Specific Manner ◽  
Time Specific ◽  
Visceral Adipose

Abstract Objectives Maternal obesity has long-term influence on metabolic health of offspring, partly through an epigenetic mechanism. Choline is a methyl donor which provides methyl groups for epigenetic modification such as DNA methylation. In this study, we examined the effect of maternal choline supplementation (MCS) on DNA methylation of offspring born to high-fat (HF) fed obese mouse dams. Methods C57BL/6J mice were fed either a 10% kcal normal fat (NF) or a 60% kcal HF diet with either 25 mM choline supplement or control drinking water from 4 weeks prior to mating until the end of gestation. The offspring were fed the HF diet for 6 weeks after weaning. We measured both global DNA methylation and site-specific methylation of several metabolic genes in the liver, visceral adipose tissue, and brain at both embryonic day E17.5 and after the post-weaning HF feeding. Results At E17.5, HF-MCS led to higher global DNA methylation in both fetal liver and brain. Methylation of one of the CpGs in the promoter region of Srebp1f (a gene that regulates lipogenesis) was also upregulated in the fetal liver by HF-MCS, accordingly there was lower expression of this gene (p < 0.05). However, HF-MCS had opposite effects on global DNA methylation after 6 weeks of post weaning HF feeding than during the fetal period. At this time point, HF-MCS led to hypomethylation of liver and visceral adipose tissue (p < 0.05). Global DNA methylation of the brain was decreased by post-weaning HF feeding but was not affected by maternal HF or MCS (p < 0.01). Conclusions In conclusion, MCS during maternal obesity in the perinatal period influences offspring DNA methylation in a time-specific manner. The epigenetic programming effect of MCS needs to be evaluated in both short and long term in the offspring. Funding Sources NIGMS.

Maternal obesity is associated with a sex-specific epigenetic programming in human neonatal monocytes

Epigenomics ◽  
2020 ◽  
Vol 12 (22) ◽  
pp. 1999-2018
Author(s):  
Fabián Vega-Tapia ◽  
Rocío Artigas ◽  
Cherie Hernández ◽  
Ricardo Uauy ◽  
Paola Casanello ◽  
...  
Keyword(s):  
Maternal Obesity ◽  
Normal Weight ◽  
Innate Immune ◽  
Blood Monocytes ◽  
Clinical Trial Registry ◽  
Epigenetic Programming ◽  
Genome Wide ◽  
Specific Analysis ◽  
Specific Manner ◽  
Maternal Bmi

Aim: To determine changes in global DNA methylation in monocytes from neonates of women with obesity, as markers of an immune programming resulting from maternal obesity. Materials & methods: Cord blood monocytes were obtained from neonates born to women with obesity and normal weight, genome-wide differentially methylated CpGs were determined using an Infinium MethylationEPIC-BeadChip (850K). Results: No clustering of samples according to maternal BMI was observed, but sex-specific analysis revealed 71,728 differentially methylated CpGs in female neonates from women with obesity (p < 0.01). DAVID analysis showed increased methylation levels within genes involved in the innate immune response and inflammation. Conclusion: Maternal obesity induces, in a sex-specific manner, an epigenetic programming of monocytes that could contribute to disease later in life. Clinical trial registry: This study is registered in ClinicalTrials.gov NCT02903134 .

scholarly journals Maternal obesity programs increased leptin gene expression in rat male offspring via epigenetic modifications in a depot-specific manner

2017 ◽  
Vol 6 (8) ◽  
pp. 922-930 ◽  
Author(s):  
Simon Lecoutre ◽  
Frederik Oger ◽  
Charlène Pourpe ◽  
Laura Butruille ◽  
Lucie Marousez ◽  
...  
Keyword(s):  
Gene Expression ◽  
Maternal Obesity ◽  
Epigenetic Modifications ◽  
Male Offspring ◽  
Specific Manner

The dual nature of obesity in metabolic programming: quantity versus quality of adipose tissue

2020 ◽  
Vol 134 (18) ◽  
pp. 2447-2451
Author(s):  
Anissa Viveiros ◽  
Gavin Y. Oudit
Keyword(s):  
Adipose Tissue ◽  
Environmental Factors ◽  
Maternal Obesity ◽  
Metabolic Programming ◽  
Dual Nature ◽  
Prevalence Of Obesity ◽  
Adipose Tissue Volume ◽  
Males And Females ◽  
Metabolically Healthy

Abstract The global prevalence of obesity has been rising at an alarming rate, accompanied by an increase in both childhood and maternal obesity. The concept of metabolic programming is highly topical, and in this context, describes a predisposition of offspring of obese mothers to the development of obesity independent of environmental factors. Research published in this issue of Clinical Science conducted by Litzenburger and colleagues (Clin. Sci. (Lond.) (2020) 134, 921–939) have identified sex-dependent differences in metabolic programming and identify putative signaling pathways involved in the differential phenotype of adipose tissue between males and females. Delineating the distinction between metabolically healthy and unhealthy obesity is a topic of emerging interest, and the precise nature of adipocytes are key to pathogenesis, independent of adipose tissue volume.

Left Ventricular Hypertrophy

2014 ◽  
Vol 19 (2) ◽  
pp. 11-15
Author(s):  
Steven L. Demeter
Keyword(s):  
Risk Factors ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Left Ventricular Mass Index ◽  
Medical Science ◽  
Careful Analysis ◽  
Left Ventricular ◽  
Hypertensive Disease ◽  
Accurate Analysis ◽  
Clear Explanation

Abstract The fourth, fifth, and sixth editions of the AMA Guides to the Evaluation of Permanent Impairment (AMA Guides) use left ventricular hypertrophy (LVH) as a variable to determine impairment caused by hypertensive disease. The issue of LVH, as assessed echocardiographically, is a prime example of medical science being at odds with legal jurisprudence. Some legislatures have allowed any cause of LVH in a hypertensive individual to be an allowed manifestation of hypertensive changes. This situation has arisen because a physician can never say that no component of LVH was not caused by the hypertension, even in an individual with a cardiomyopathy or valvular disorder. This article recommends that evaluators consider three points: if the cause of the LVH is hypertension, is the examinee at maximum medical improvement; is the LVH caused by hypertension or another factor; and, if apportionment is allowed, then a careful analysis of the risk factors for other disorders associated with LVH is necessary. The left ventricular mass index should be present in the echocardiogram report and can guide the interpretation of the alleged LVH; if not present, it should be requested because it facilitates a more accurate analysis. Further, if the cause of the LVH is more likely independent of the hypertension, then careful reasoning and an explanation should be included in the impairment report. If hypertension is only a partial cause, a reasoned analysis and clear explanation of the apportionment are required.

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