Chronic exposure to environmental noise has been increasingly linked to metabolic and cardiovascular diseases. Epidemiological data suggest that each 10 dB increase in road traffic noise corresponds to an 11% higher risk of developing type 2 diabetes mellitus (T2DM), yet the mechanistic basis of this relationship remains poorly defined. This study aims to establish a physiologically relevant animal model to investigate how subchronic exposure to continuous noise contributes to metabolic dysregulation and to identify early biomarkers of preadiposity and prediabetes.
Twelve-week-old male and female C57BL/6J wild-type mice were exposed continuously to aircraft noise at a mean sound pressure level of 72 dB(A) for four weeks. Blood pressure and body weight were recorded weekly, and postmortem analyses were performed to assess oxidative stress, metabolic markers, inflammatory & stress responses. Functional analyses of electrically stimulated isolated cardiomyocytes (e.g. contraction times) and high-resolution respirometry were used to characterize noise-induced damage of the heart.
Noise-exposed animals exhibited sustained elevation in blood pressure, more pronounced endothelial dysfunction and attenuated body weight gain compared to controls. In noise-exposed male mice, cardiac tissue displayed decreased maximum mitochondrial respiration compared to the controls, indicating functional impairment of the respiratory chain. Both oxidative stress and inflammatory marker expression in the heart were increased in noise-exposed groups compared to controls. Plasma analyses revealed a trend toward higher hypothalamic-pituitary-adrenal (HPA) axis activity and metabolic marker levels in both sexes.
Collectively, these findings suggest that subchronic aircraft noise exposure induces systemic physiological stress and early metabolic alterations, supporting the hypothesis that environmental noise contributes to prediabetic changes via oxidative and inflammatory mechanisms, also affecting islet function. Ongoing analyses aim to delineate sex-specific responses and identify predictive circulating biomarkers for noise-induced metabolic dysfunction. This study lays a solid foundation for further exploring the noise effect in diabetic and metabolically challenged animal models.
