Journal
NUTRIENTS
Volume 9, Issue 4, Pages -Publisher
MDPI
DOI: 10.3390/nu9040407
Keywords
cardiometabolic disease; chromatin-immunoprecipitation sequencing; developmental programing; histone modifications; maternal high-fat diet
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Funding
- Sanford Health-South Dakota State University Collaborative Research program
- S.D. Board of Regents RAMP
- D Innovation program
- National Institutes of Health [600 (NIH)-NICHD K08HD078504]
- SSOM-USD Faculty Grant
- USDA National Institute of Food and Agriculture [1004817]
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Infants born to women with diabetes or obesity are exposed to excess circulating fuels during fetal heart development and are at higher risk of cardiac diseases. We have previously shown that late-gestation diabetes, especially in conjunction with a maternal high-fat (HF) diet, impairs cardiac functions in rat-offspring. This study investigated changes in genome-wide histone modifications in newborn hearts from rat-pups exposed to maternal diabetes and HF-diet. Chromatin-immunoprecipitation-sequencing revealed a differential peak distribution on gene promoters in exposed pups with respect to acetylation of lysines 9 and 14 and to trimethylation of lysines 4 and 27 in histone H3 (all, false discovery rate, FDR <0.1). In the HF-diet exposed offspring, 54% of the annotated genes showed the gene-activating mark trimethylated lysine 4. Many of these genes (1) are associated with the metabolic process in general and particularly with positive regulation of cholesterol biosynthesis (FDR = 0.03); (2) overlap with 455 quantitative trait loci for blood pressure, body weight, serum cholesterol (all, FDR < 0.1); and (3) are linked to cardiac disease susceptibility/progression, based on disease ontology analyses and scientific literature. These results indicate that maternal HF-diet changes the cardiac histone signature in offspring suggesting a fuel-mediated epigenetic reprogramming of cardiac tissue in utero.
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