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A Murine Pancreatic Islet Cell-based Screening for Diabetogenic Environmental Chemicals
Published on: June 25, 2018
Maternal exposure to air pollution and umbilical asprosin concentration, a novel insulin-resistant marker
Zeynab Sadat Hosseini1, Hafez Heydari-Zarnagh1, Moslem Lari Najafi2
1Cellular and Molecular Research Center, Sabzevar University of Medical Sciences, Sabzevar, Iran.
Abstract:
Air pollution exposure during pregnancy has been associated with abnormal glucose hemostasis in the fetus, which may result in the programming of type 2 diabetes mellitus (T2DM) development in future life. Therefore, we investigated the association of maternal exposure to particulate matters (PMs) and traffic indicators with umbilical asprosin concentration, a novel insulin-resistant inducing adipokine, in newborns. Accordingly, 759 mother-newborn pairs from Sabzevar, Iran (2018-2019) participated in our study. Maternal exposure to PM1, PM2.5 and PM10 concentrations was estimated using spatial-temporal models developed for the study area. The associations of exposure to traffic indicators (total street length in 100, 300 and 500 m buffers around home and proximity of mothers to nearest major roads) and air pollution with umbilical asprosin concentration were estimated using linear regression models, adjusted for potential confounders. The median (interquartile range (IQR)) of umbilical asprosin concentration was 30.4 (19.1) ng/mL. In fully adjusted models, each one IQR increase in PM10 and PM2.5 were associated with 26.43 ng/mL (95% CI: 10.97, 41.88) and 31.76 ng/mL (95% CI: 15.66, 47.86) increase in umbilical asprosin concentration, respectively. A similarity result was observed for total street length in 100 m buffer. An increase in proximity to major roads was associated with a decrease of -21.48 ng/mL (95% CI: 33.29, -9.67) in umbilical asprosin concentration. Our results suggested that maternal exposure to air pollution during pregnancy could increase the umbilical asprosin concentration. These novel findings may improve our understanding of the mechanisms whereby air pollutants impaired glucose hemostasis during the fetal period.
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