Maternal early mid-pregnancy adiponectin in relation to infant birth weight and the likelihood of being born large-for-gestational-age

Abstract

This study aimed to evaluate the association of maternal adiponectin with infant birth size in 1349 pregnant women at Uppsala University Hospital, Sweden. The mean age of the women was 31.0 years, and 40.9% were nulliparous. Maternal early mid-pregnancy adiponectin was measured in microgram/mL. Linear regression models were performed to evaluate the association between adiponectin and infant birth weight. Logistic regression models were used to evaluate adiponectin in relation to the odds of giving birth to an infant large-for-gestational-age (LGA, infant birth weight standard deviation score > 90th percentile). Adjustments were made for early pregnancy BMI and diabetes mellitus. Prior adjustments, adiponectin was inversely associated with infant birth weight (β − 17.1, 95% confidence interval (CI) − 26.8 to − 7.4 g, P < 0.001), and one microgram/mL increase in adiponectin was associated with a 9% decrease in the odds of giving birth to an LGA infant (odds ratio 0.91, CI 0.85–0.97, P = 0.006). The associations did not withstand in the adjusted models. We found a significant interaction between adiponectin and infant sex on birth size. This interaction was driven by an inverse association between maternal adiponectin and birth size in female infants, whereas no such association was found in males.

Maternal obesity: sex‐specific in utero changes in fetal brain autophagy and mTOR

“…Although maternal adiponectin does not cross the blood‐placental barrier, both adiponectin and adiponectin receptors (ADIPOR1 and ADIPOR2) are expressed by placental cells. There is evidence that adiponectin inhibits the expression of glucose and amino acid transporters in placental cells, limiting nutrient availability for the fetus [17]. However, adiponectin is known to cross the blood–brain barrier, impacting brain signaling related to food intake and energy expenditure [18, 19].…”