Monochromatic blue light not green light exposure is associated with continuous light-induced hepatic steatosis in high fat diet fed-mice via oxidative stress

Irregular light exposure is a newly identified environmental factor for the progression of lipid metabolism; however, the specific effect of light color exposure on lipid homeostasis remains unknown. Herein, 4-week-old male C57BL/6 J mice (n = 12) fed a high-fat diet (HFD) were exposed to a standard 12-h light: 12-h dark cycle (LD-WF) and a 24-h continuous monochromatic blue light (LL-BF), green light (LL-GF), or white light (LL-WF) condition for 12 weeks. LL-BF interfered with the expression of circadian genes in the hypothalamus and upregulated the plasma corticosterone (CORT) levels (p < 0.05) compared with LD-WF. Along with elevation of the CORT level, LL-BF enhanced glucocorticoid receptor synthesis, increased the Hsp90 mRNA level, reduced the antioxidant capacity, increased the production of ROS and MDA, and reduced the Pgc-1 alpha mRNA level in the liver (p < 0.05). Furthermore, LL-BF disrupted the hepatic expression levels of genes involved in lipid metabolism, Acc and Hl, which further aggravated the hepatic steatosis status and significantly increased the liver pathological scores, TG, TC, IL-6, and TNF-alpha levels (p < 0.05). LL-BF consistently increased the body weight and incidence of dyslipidemia and lipid deposition. However, no difference was observed between LL-BF and LL-WF (p > 0.05). Surprisingly, LL-GF did not show any changes induced by LL-BF and LL-WF, and contrary to LL-BF, LL-GF and LD-WF showed no significantly differing changes (p > 0.05). Taken together, exposure to monochromatic blue light but not green light is associated with continuous light-aggravated hepatic steatosis in HFD-fed mice. The effect of continuous blue light exposure may be attributed to the disturbance of biological rhythm, increase in CORT secretion, induction of oxidative stress, and interference of the Acc and Hl levels in the liver.