Associations of maternal diet and placenta leptin methylation

• Published in: Molecular and cellular endocrinology Vol. 505; p. 110739
• Main Authors: Daniels, Teresa E., Sadovnikoff, Alexander I., Ridout, Kathryn K., Lesseur, Corina, Marsit, Carmen J., Tyrka, Audrey R.
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier B.V 05.04.2020
• Subjects: Adult; Diet; DNA Methylation - genetics; Epigenetics; Female; Humans; Infant, Newborn; Leptin; Leptin - genetics; Linear Models; Male; Maternal nutrition; Methylation; Models, Biological; Nutrients - metabolism; Placenta; Placenta - metabolism; Pregnancy; Epigenetics; Placenta; Diet; Methylation; Leptin; Maternal nutrition
• ISSN: 0303-7207; 1872-8057
• DOI: 10.1016/j.mce.2020.110739

Maternal diet is an important factor in prenatal development that also has implications for disease risk later in life. The adipokine leptin is a key regulator of energy homeostasis and may be involved in the association between maternal nutrition, maternal obesity, and infant outcomes. DNA methylation of placenta genes may occur in response to exposures and may program subsequent infant development. This study examined maternal diet, placenta leptin gene DNA methylation, and neonatal growth in a sample of healthy neonates and their mothers. Mothers and their healthy neonates (N = 135) were recruited within 1–2 days following delivery at Women and Infants Hospital in Providence, RI. A structured interview was conducted to assess maternal dietary intake. Maternal pre-pregnancy weight, weight gain during pregnancy, maternal health, medications, and vitamin use were obtained from medical records. Bisulfite pyrosequencing was used to measure methylation of CpG sites in the promoter region of the placenta leptin gene and determine genotype of the leptin single nucleotide polymorphism (SNP) rs2167270, which is known to influence leptin methylation. Bivariate analyses and linear regression models were used to evaluate associations of demographics, diet, and mean leptin methylation. Genotype was a significant predictor of placenta leptin DNA methylation (p < .01), and after controlling for this and other relevant maternal and infant covariates, lower levels of leptin methylation were significantly associated with greater intake of carbohydrates (p < .05), in particular added sugars (p < .05) and white/refined carbohydrates (p < .05). Total caloric intake was also associated with placenta leptin methylation (p < .05), however after controlling for relevant covariates, significance diminished to trend-level. There were no significant associations of placenta leptin methylation and intake of protein (p > .05) or fat (p > .05). These findings underline the importance of intake of carbohydrate consumption for methylation of the placenta leptin gene. Because methylation reduces gene transcription, lower methylation may indicate a placenta response to high caloric intake and carbohydrate food that would result in higher levels of this hormone during fetal development. Further investigation of the developmental ramifications of epigenetic changes to placenta leptin methylation should be pursued. •Maternal intake of carbohydrates is negatively predictive of placenta leptin methylation.•Among carbohydrates, sugars and white/refined carbohydrates, but not whole wheat carbohydrates were negatively predictive.•These findings withstood correction for potential mediators of placenta leptin methylation.•Maternal intake of fat and protein did not demonstrate associations with placenta leptin methylation.