Article Text

  1. M H Fasting1,2,
  2. E Oken2,
  3. C S Mantzoros3,
  4. J W Rich-Edwards2,4,5,
  5. K Kleinman2,
  6. S L Rifas-Shiman2,
  7. T Vik1,
  8. M W Gillman2,6
  1. 1Department of Public Health and General Practice, The Norwegian University of Science and Technology, Medisinsk Teknisk Forskningssenter, Trondheim, Norway
  2. 2Obesity Prevention Program, Department of Ambulatory Care and Prevention, Harvard Medical School and Harvard Pilgrim Health Care, Boston, MA, USA
  3. 3Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA
  4. 4Connors Center for Women’s Health and Gender Bioogy, Brigham and Women’s Hospital, Boston, MA, USA
  5. 5Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA
  6. 6Department of Nutrition, Harvard School of Public Health, Boston, MA, USA


Background Fetal glucocorticoid exposure is associated with later development of features of the metabolic syndrome such as hypertension and abdominal obesity. Fat tissue produces adiponectin and leptin, hormones with effects on energy consumption and metabolism. It is unclear how fetal glucocorticoid exposure influences secretion of these adipokines.

Aim To study the relationship of maternal mid pregnancy corticotropin releasing hormone (CRH) levels, a proxy of fetal glucocorticoid exposure, with offspring levels of adiponectin and leptin in early childhood.

Methods The study population consisted of 355 mother-children pairs from Project Viva, a prospective pre birth cohort study from eastern Massachusetts, USA. We created a general linear model with log CRH levels in mid pregnancy maternal blood as the predictor and adiponectin and leptin measured in the 3 year old offspring as outcomes, adjusting for maternal and child characteristics.

Results Mean (SD) log CRH was 4.98 (0.61) log pg/ml, adiponectin 22.3 (5.7) μg/ml and leptin 1.9 (1.8) ng/ml. After adjustment for maternal race/ethnicity, pregnancy induced hypertension, age at check up and sex, each unit increment in log CRH mean offspring adiponectin was 1.05 μg/ml (95% CI: 0.02 to 2.08) higher. We found no association with leptin (−0.07 ng/ml, 95% CI: −0.39 to 0.25). Leptin was associated with BMI (r = 0.21, p<0.001), while adiponectin was not (r = 0.07, p = 0.22).

Conclusions Higher maternal blood levels of CRH were associated with higher offspring levels of adiponectin at age 3 years, a finding which might indicate that children with high fetal glucocorticoid exposure are more insulin resistant.

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