期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 21, 期 1, 页码 -出版社
MDPI
DOI: 10.3390/ijms21010329
关键词
childhood obesity; skinfolds thickness; BMI; epigenetics; fetal programming; maternal hyperglycemia; pregnancy
资金
- American Diabetes Association [1-15-ACE-26]
- Fonds de recherche du Quebec en sante (FRSQ) [20697]
- Canadian Institute of Health Research [MOP 115071]
- Diabete Quebec grants
Changes in fetal DNA methylation (DNAm) of the leptin (LEP) gene have been associated with exposure to maternal hyperglycemia, but their links with childhood obesity risk are still unclear. We investigated the association between maternal hyperglycemia, placental LEP DNAm (25 5 '-C-phosphate-G-3 ' (CpG) sites), neonatal leptinemia, and adiposity (i.e., BMI and skinfold thickness (ST) (subscapular (SS) + triceps (TR) skinfold measures, and the ratio of SS:TR) at 3-years-old, in 259 mother-child dyads, from Gen3G birth cohort. We conducted multivariate linear analyses adjusted for gestational age at birth, sex of the child, age at follow-up, and cellular heterogeneity. We assessed the causal role of DNAm in the association between maternal glycemia and childhood outcomes, using mediation analysis. We found three CpGs associated with neonatal leptinemia (p <= 0.002). Of these, cg05136031 and cg15758240 were also associated with BMI (beta = -2.69, p = 0.05) and fat distribution (beta = -0.581, p = 0.05) at 3-years-old, respectively. Maternal glycemia was associated with DNAm at cg15758240 (beta = -0.01, p = 0.04) and neonatal leptinemia (beta = 0.19, p = 0.004). DNAm levels at cg15758240 mediates 0.8% of the association between maternal glycemia and neonatal leptinemia (p < 0.001). Our results support that DNAm regulation of the leptin pathway in response to maternal glycemia might be involved in programming adiposity in childhood.
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