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) microg/ml, and 1.9 (1.8) ng/ml. For each unit increment in log CRH, mean value of offspring adiponectin was 1.10 microg/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.
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) microg/ml, and 1.9 (1.8) ng/ml. For each unit increment in log CRH, mean value of offspring adiponectin was 1.10 microg/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.
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