Cited by 210Birth, Development, and HealthEpigenetics and DNA MethylationGestational Diabetes Research and Management

Placental Adiponectin Gene DNA Methylation Levels Are Associated With Mothers’ Blood Glucose Concentration

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Bouchard, Luigi, Hivert, Marie-France, Guay, Simon-Pierre, St-Pierre, Julie, Perron, Patrice, Brisson, Diane·2012·Diabetes

Abstract

Growing evidence suggests that epigenetic profile changes occurring during fetal development in response to in utero environment variations could be one of the mechanisms involved in the early determinants of adult chronic diseases. In this study, we tested whether maternal glycemic status is associated with the adiponectin gene (ADIPOQ) DNA methylation profile in placenta tissue, in maternal circulating blood cells, and in cord blood cells. We found that lower DNA methylation levels in the promoter of ADIPOQ on the fetal side of the placenta were correlated with higher maternal glucose levels during the second trimester of pregnancy (2-h glucose after the oral glucose tolerance test; rs ≤ −0.21, P < 0.05). Lower DNA methylation levels on the maternal side of the placenta were associated with higher insulin resistance index (homeostasis model assessment of insulin resistance) during the second and third trimesters of pregnancy (rs ≤ −0.27, P < 0.05). Finally, lower DNA methylation levels were associated with higher maternal circulating adiponectin levels throughout pregnancy (rs ≤ −0.26, P < 0.05). In conclusion, the ADIPOQ DNA methylation profile was associated with maternal glucose status and with maternal circulating adiponectin concentration. Because adiponectin is suspected to have insulin-sensitizing proprieties, these epigenetic adaptations have the potential to induce sustained glucose metabolism changes in the mother and offspring later in life.

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  • Adiponectin gene methylation in the placenta is associated with maternal glucose intolerance and fetal macrosomia.

    “Therefore, adiponectin gene methylation in the placenta is associated with maternal glucose intolerance and fetal macrosomia [108].”

    From The Pathophysiology of Gestational Diabetes Mellitus (2018) · cites this paper as [108]

    The Discussion (page unavailable) reports that placental ADIPOQ methylation was associated with maternal glucose metabolism across both normal and impaired glucose tolerance. The Results and Discussion discuss birth weight in relation to cord-blood adiponectin, not placental ADIPOQ methylation; our copy does not establish an association between that methylation and fetal macrosomia. (LLM, conf=0.88)

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References 52 · Cited by 210

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Authors
Bouchard, L., Hivert, M.-F., Guay, S.-P., St-Pierre, J., Perron, P., & Brisson, D.
Affiliations
  • Université de Sherbrooke (CA)
  • Faculty of Pharmacy, Université Laval, Québec City, Québec Canada
  • Hôpital de Chicoutimi (CA)
Corresponding author
Bouchard, Luigi
Venue
Diabetes
Published
2012-04-13
Volume
61
Issue
5
Pages
1272-1280
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
OpenAlex
W2115371848
Cited by
210
References
52
Citations by year
2026: 3 · 2025: 5 · 2024: 10 · 2023: 11 · 2022: 16 · 2021: 16 · 2020: 14 · 2019: 12 · 2018: 27 · 2017: 10 · 2016: 9 · 2015: 26 · 2014: 25 · 2013: 13 · 2012: 11
FWCI
21.09
Type
journal article
Language
en
Open access
Locations
  • Diabetes (publishedVersion, cc-by-nc-nd)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
  • Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
Keywords
adiponectin, ADIPOQ, DNA methylation, placenta, maternal blood glucose, insulin resistance, umbilical cord blood, epigenetics, fetal programming, oral glucose tolerance test, HOMA-IR
MeSH terms
Adult, Blood Glucose, Erythrocytes, Female, Fetal Blood, Humans, Placenta, Pregnancy, Diabetes, Gestational, Gene Expression Regulation, Developmental, DNA Methylation, Epigenesis, Genetic, Adiponectin, Young Adult

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