Circadian desynchronization induces diabetes-like conditions in gestational female syrian hamsters.

Altered light exposure is an emerging risk factor for metabolic health; however, its effects on maternal physiology and pregnancy outcomes remain poorly understood. This study examined the effects of reversing the natural light-dark cycle (12 h dark:12 h light) during pregnancy in hamsters to mimic shift light exposure in human shift workers and assess associated metabolic changes during mid (10.5 days) and late gestation (14.5 days). Our results suggest that shift of light (SL) altered histomorphology, showing sinusoidal congestion, distorted liver architecture, and increased lipid accumulation in adipose tissue. Ultrasound and PAI showed impaired uteroplacental function, retarded fetal growth and reduced oxygenation of implantation sites. SL further disrupted circadian rhythms, gestational weight gain, glucose tolerance, and metabolic stress. SL reduced implantation, irregular embryo spacing, and increased body weight compared to NDL. Oral glucose tolerance test (OGTT) showed impaired glucose clearance and hyperglycemia in SL during late gestation. SL decreased SOD/Catalase enzyme activity, suggesting increased oxidative stress. Western blot showed altered GLUT2 and GLUT4 protein expression in the liver and adipose tissue. SL altered the rhythmicity of the circadian protein Cry1 in the liver. qPCR revealed that SL affected clock genes (Bmal1, Per1, Per2, and Cry1) in the SCN, liver, and adipose tissue, indicating misalignment of central and peripheral clock gene rhythms. Our findings suggest that light-induced circadian disruption during pregnancy leads to metabolic dysfunction, increased oxidative stress, and altered clock gene expression in maternal liver and adipose tissues, potentially contributing to adverse gestational outcomes in the hamster.