This Article Full Text Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Fasting, M. H. Articles by Gillman, M. W. Search for Related Content PubMed PubMed Citation Articles by Fasting, M. H. Articles by Gillman, M. W. Related Collections Adrenal and Hypertension Neuroendocrinology and Pituitary Pediatric Endocrinology Metabolism

Maternal Levels of Corticotropin-Releasing Hormone during Pregnancy in Relation to Adiponectin and Leptin in Early Childhood

Department of Public Health and General Practice (M.H.F., T.V.), The Norwegian University of Science and Technology, 7489 Trondheim, Norway; Obesity Prevention Program (M.H.F., E.O., J.W.R.-E., K.K., S.L.R.-S., M.W.G.), Department of Ambulatory Care and Prevention, Harvard Medical School and Harvard Pilgrim Health Care, and Boston, Division of Endocrinology, Diabetes, and Metabolism (C.S.M.), Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Massachusetts 02215; and Division of Endocrinology (J.A.M.), Children’s Hospital, Harvard Medical School; Connors Center for Women’s Health and Gender Biology (J.W.R.-E.), Brigham and Women’s Hospital; and Departments of Epidemiology (J.W.R.-E.) and Nutrition (M.W.G.), Harvard School of Public Health, Boston, Massachusetts 02115

Address all correspondence and requests for reprints to: Magnus H. Fasting, Medisinsk Teknisk Forskningssenter, 7489 Trondheim, Norway. E-mail: magnus.fasting{at}gmail.com.

Background: Fetal glucocorticoid exposure is associated with later development of features of the metabolic syndrome such as central obesity and insulin resistance. Fat tissue, especially visceral fat, produces adiponectin, which is inversely associated with insulin resistance in older children and adults. Adipocytes also produce leptin, directly related to measures of adiposity. It is unknown how the secretion of these hormones in early childhood is related to pregnancy levels of CRH, a proxy of fetal glucocorticoid exposure.

Aim: Our aim was to study the relationship of maternal midpregnancy CRH levels with offspring levels of adiponectin and leptin in early childhood.

Methods: The study population consisted of 349 mother-children pairs from Project Viva, a prospective prebirth cohort study from eastern Massachusetts. We created a general linear model with log CRH levels in midpregnancy maternal blood as the predictor and adiponectin and leptin measured in the 3-yr-old offspring as outcomes, adjusting for covariates.

Results: The means (SD) of log CRH, adiponectin, and leptin were 4.97 (0.65) log pg/ml, 22.4 (5.8) µg/ml, and 1.9 (1.8) ng/ml. For each unit increment in log CRH, mean value of offspring adiponectin was 1.10 µg/ml (95% confidence interval = 0.06–2.14) higher. We found no association with leptin (–0.08 ng/ml; 95% confidence interval = –0.40–0.24).

Conclusions: Higher maternal blood levels of CRH were associated with higher levels of adiponectin but unchanged levels of leptin at age 3 yr. The increased adiponectin levels might represent secretion from organs other than fat or reflect a compensatory mechanism to increase insulin sensitivity.