Blue light exposure exacerbates obesity in high-fat diet-fed mice by inducing mitochondrial dysfunction in the white adipose tissue.

Abstract

The increasing prevalence of artificial light sources has rendered blue light (BL) a novel environmental metabolic disruptor. This study aimed to investigate the potential effects of BL exposure on mitochondrial function in the adipose tissue of high-fat diet (HFD) mice. A total of 36 mice were divided into the normal diet (ND) and HFD groups and subsequently exposed to white light (WL) and BL. Body weight was monitored regularly, and glucose tolerance and insulin sensitivity were assessed using intraperitoneal glucose tolerance tests (IPGTT) and intraperitoneal insulin tolerance tests (IPITT). Body fat was measured using nuclear magnetic resonance, and overall energy metabolism was evaluated using a metabolic energy monitoring system. After the mice were humanely sacrificed, inguinal white adipose tissue (iWAT), epididymal white adipose tissue (eWAT), and brown adipose tissue (BAT) were collected for weighing, histological analysis, and serum biochemical analysis. Oxidative stress indicators were detected by flow cytometry and other methods. We found that, in HFD-fed mice, BL exposure significantly increased body weight and body fat, exacerbated insulin resistance, and reduced oxygen consumption and thermogenesis. Transcriptomic analysis revealed that BL exposure induced oxidative stress in the white adipose tissue and suppressed the oxidative phosphorylation pathway. RT-qPCR and western blotting of the iWAT confirmed the downregulation of key genes in this pathway. Collectively, our results suggest that BL may target the adipose tissue, trigger oxidative stress, suppress oxidative phosphorylation, impair mitochondrial function, and exacerbate obesity.