Chronic irregular photoperiod disrupts locomotor rhythms and hypothalamic clock gene expression without metabolic imbalance in the male volcano mouse <i>Neotomodon alstoni</i>

Circadian rhythms in physiology are coordinated daily variations driven by endogenous oscillators and synchronized by environmental light-dark cycles. Chronic disruption of the natural photoperiod has been associated with circadian desynchronization and physiological impairment. To examine these effects, we exposed adult lean male <i>Neotomodon alstoni</i> to an irregular photoperiod composed of alternating short and long cycles over a week, with abrupt phase shifts and maintained for three consecutive months. Behavioral, physiological, and molecular parameters were assessed, focusing on hypothalamic expression of circadian clock genes (<i>Per1, Bmal1</i>), metabolic regulators (<i>Mchr1, Crh, Prepro-orexin, Sirt1</i>), and feeding-related genes (<i>Npy, Lepr</i>). The irregular photoperiod differentially altered locomotor rhythms depending on phase delays or advances and increased food consumption during the photophase. Nocturnal expression of clock and metabolism-related genes was also modified in the hypothalamus. However, body weight, total food intake, and glucose handling remained unchanged. These findings indicate that in <i>N. alstoni</i>, chronic exposure to an irregular photoperiod disrupts circadian organization of activity and hypothalamic gene expression suggesting that a compensatory mechanisms may preserve overall metabolic homeostasis.