Particulate Matter Exposure During Perinatal Life Results in Impaired Glucose Metabolism in Adult Male Rat Offspring

Abstract

Background/Aims: Particulate matter (PM) is an important risk factor for immunological system imbalance due to its small size, which can reach more distal regions of the respiratory tract, independently of its chemical composition. Some studies have suggested that PM exposure is associated with an increased incidence of diabetes, especially in industrialized urban regions. However, studies regarding the effects of PM exposure during perinatal life on glucose metabolism are limited. We tested whether exposure to PM from an urban area with poor air quality during pregnancy and lactation could cause short- and long-term dysfunction in rat offspring. Methods: Samples of < 10 µm PM were collected in an urban area of Cotonou, Benin (West Africa), and reconstituted in corn oil. Pregnant Wistar rats received 50 µg PM/day by gavage until the end of lactation. After birth, we analyzed the dams’ biochemical parameters as well as those of their male offspring at 21 and 90 days of age. Results: The results showed that PM exposure did not lead to several consequences in dams; however, the male offspring of both ages presented an increase of approximately 15% in body weight. Although the blood glucose levels remained unchanged, the insulin levels were increased 2.5- and 2-fold in PM exposure groups of both ages, respectively. HOMA-IR and HOMA-β were also increased at both ages. We also demonstrated that the number, islet area and insulin immunodensity of pancreatic islets were significantly increased at both ages from PM exposure. Conclusion: Our data show that chronic PM exposure by the oral route during perinatal life in rats leads to glucose dyshomeostasis in male offspring both in early and later life. Thus, we suggest that an ambience with poor air quality, mainly where traffic is dense, can contribute to an increase in metabolic disease incidence.

Preconception air pollution exposure and glucose tolerance in healthy pregnant women in a middle-income country

“…A rat model study by Yi et al 2017 showed that exposure to PM 2.5 has reduced pancreas glucose transporter2 (GLUT2) expression as one of the important factor of glucose intolerance as well as pancreatic methane dicarboxylic aldehyde (MDA) and suggested that inflammation and oxidative stress response related exposure to PM 2.5 could increase risk of pancreatic impairment and glycemic consequence [65]. Other animal studies also reported that exposure to air pollution had been associated with increase in insulin immunodensity of pancreatic islets [66,67]. Finally, changes in glucose homeostasis in healthy pregnant women might be due to the metabolic induction change in the hypothalamus [68,69].…”

Prenatal Pollutant Exposures and Hypothalamic Development: Early Life Disruption of Metabolic Programming

“…As the onset of metabolic disorders steadily increases in children and young adults, there is a great need to understand this etiology. Significant associations have been found between prenatal exposure to environmental pollutants and the heightened risk for metabolic impairments ( 69 , 71 , 73 , 125 ). One potential mechanism is an increase in neuroinflammation, particularly affecting the hypothalamus.…”

Preconception air pollution exposure and glucose tolerance in healthy pregnant women in a middle-income country

“…A rat model study by Yi et al 2017 showed that exposure to PM 2.5 has reduced pancreas glucose transporter2 (GLUT2) expression as one of the important factor of glucose intolerance as well as pancreatic methane dicarboxylic aldehyde (MDA) and suggested that in ammation and oxidative stress response related exposure to PM 2.5 could increase risk of pancreatic impairment and glycemic consequence [65]. Other animal studies also reported that exposure to air pollution had been associated with increase in insulin immunodensity of pancreatic islets [66,67]. Finally, changes in glucose homeostasis in healthy pregnant women might be due to the metabolic induction change in the hypothalamus [68,69].…”