Maintaining the normal biological rhythms of livestock is of great significance for reflecting the environmental suitability and welfare level of animals. Mistimed feeding can interfere with the circadian rhythms of both humans and animals, resulting in disorders of lipid metabolism, obesity, and metabolic syndrome. Low-temperature environment stimulates increased appetite and decreased physical activity, resulting in higher energy intake than consumption and thus facilitating fat deposition and even obesity. In this study, growing rabbits were randomly allocated to the daytime feeding (DF) group and nighttime restricted feeding (NRF) group. Our research demonstrated that, during winter, the DF regimen disrupted the behavioral rhythms of rabbits and accelerated weight gain without changing overall feed intake. The underlying reason was that DF disturbed the lipid metabolism rhythms, promoted hepatic lipid synthesis regulated by DGAT1 and lipid synthesis of adipose tissues regulated by GPAM, thus triggering fat deposition. In contrast, the NRF regimen enhanced thermogenesis regulated by T3 and elevated body temperature and facilitated ketogenesis mediated by HMGCS2, increasing energy consumption. However, it had no significant impact on the fat content within muscle. This study offers a theoretical foundation for the refinement of feeding management and healthy raising of rabbits.

This study compared a programmable logic controller (PLC) combining indoor temperature, outdoor temperature, and outdoor relative humidity with conventional temperature-triggered pad cooling and manual fan adjustment in two commercial rabbit houses in Leshan, China, a region characterized by a hot and humid climate. The 33-day summer trial included 108 selected Hyla rabbits aged 39 d per house. The PLC house had a mean air temperature 0.36 °C higher and relative humidity 4.34 percentage points lower than the control house. Final body weight and average daily gain were higher, while feed conversion did not differ significantly. Intra-abdominal temperature near the cooling pads was 0.29 °C lower. Estimated cooling pad recirculation was 81.0% lower and combined fan and pump electricity use was 21.2% higher. A partial-budget analysis at a standardized scale of 3000 retained rabbit production-equivalents estimated a benefit 2955.95 Chinese yuan (CNY) higher for the treatment house than for the control house under the specified prices and scaling assumptions. Each strategy was applied in one house, so these preliminary differences cannot be separated from house effects. These observations support further evaluation in independently replicated houses, with animal responses, resource use, and deployment costs assessed together.

D-box binding protein (DBP) is a high-amplitude proline- and acidic amino acid-rich basic leucine zipper (PAR bZIP) transcription factor that functions as a key circadian output regulator downstream of the core molecular clock. Although DBP is widely recognized as a clock-controlled gene, its broader role in converting circadian timing into tissue-specific physiological programs remains incompletely integrated. In this review, we synthesize current evidence supporting DBP as a context-dependent D-box-centered regulatory node. We first summarize the upstream mechanisms that establish rhythmic Dbp expression, including CLOCK–BMAL1-dependent transcription, promoter-level amplification, signaling-dependent modulation, and post-translational control of DBP stability. We then discuss how DBP, together with related PAR bZIP activators and the opposing repressor E4 promoter-binding protein 4/nuclear factor interleukin 3 regulated (E4BP4/NFIL3), regulates D-box-mediated transcriptional output. Finally, we examine tissue-selective DBP functions in hepatic metabolism, pancreatic β-cell secretory competence, neural and behavioral regulation, reproductive neuroendocrine timing, and T helper 9 (Th9)-associated antitumor immunity. Across these systems, DBP does not act as a universal circadian effector; rather, its function depends on chromatin accessibility, cofactor availability, competing transcription factors, and local signaling context. We also highlight the current limits of human translational evidence and propose that DBP-centered signatures may be useful for interpreting circadian output failure in disease. Overall, DBP provides a mechanistically informative framework for understanding how circadian time is transformed into organ-specific physiological function and pathological vulnerability.