Abstract
Humans are increasingly affected by circadian disruption due to light pollution, which likely increases the risk of metabolic disorders. It is still difficult, however, to dissociate the effects induced by indoor light at night (LAN) from those induced by circadian desynchronization, especially in women who are underrepresented in studies. For that purpose, we compared metabolic and circadian consequences of a 10-week exposure to either chronic LAN (light at night 4 days/week, mimicking nightwork) or chronic night shift (CNS, weekly 10-h shift of the light-dark cycle mimicking shiftwork) to the regular light-dark cycle (control group) in a female diurnal rodent, Arvicanthis ansorgei, an animal model for human pathophysiology. Both CNS- and LAN-exposed Arvicanthis gained more body mass than controls and lost daily rhythmicity of various forms of albumin and metabolic gene expression in the liver. Plasma levels of glycated albumin, a glycemic control marker, were specifically increased in the LAN-exposed group. However, only individuals exposed to CNS displayed increased fasting glucose, impaired glucose tolerance, increased plasma LDL-cholesterol, and marked alterations in daily rhythms of rest-activity and feeding. Clock gene expression in the suprachiasmatic nuclei of the hypothalamus and liver was more markedly altered after CNS than LAN. Overall, these data indicate that exposure to CNS is more harmful than chronic LAN on various circadian and metabolic parameters in a female diurnal rodent, CNS triggering risk factors for atherosclerosis and diabetes. Further studies are needed to find chronotherapeutic countermeasures to prevent impaired liver metabolic rhythms after both LAN and CNS and CNS-induced circadian misalignment.