![]() ![]() We have been investigating this syndrome in a unique animal model, the fat sand rat ( Psammomys obesus). Such circadian disruption in animal models, as well as in humans, may lead to the “circadian syndrome,” with depressive-like behavior 13, CVD 9, and T2DM 13. Importantly, there is increasing recognition that pathological misalignment of network components-between the environment, behavior, SCN, and peripheral clocks (e.g., in shiftwork and jet lag) -has critical implications not only for an individual’s health and performance but also for the pathophysiology of aging and disease 9, 10, 11, 12. ![]() This network of clocks is capable of adaptively re-aligning its oscillatory components under changing conditions, including to signals such as, e.g., temperature, blood glucose and oxygen levels, and glucocorticoids. In mammals, a “central” or “master” clock in the hypothalamus of the brain (suprachiasmatic nucleus ) synchronizes “peripheral” clocks found in cells, tissues, and organs throughout the brain and body to regulate metabolism and temporal physiology 7, 8. Emerging evidence suggests that disruption of circadian rhythmicity may contribute to the development of these comorbidities, and we have proposed the term "circadian syndrome" for this combined pathological condition 5, 6.Ĭircadian rhythms are the manifestation of an internal timekeeping system (the “circadian clock ”) that is re-set (entrained) through daily environmental timing cues, especially light but also feeding and physical activity, allowing living things to anticipate periodic daily events, to orchestrate internal temporal programs of behavioral and physiological functions, and to flexibly set the order and scheduling of such functions to optimize fitness in the real world. The comorbidity between depression, cardiovascular diseases (CVD), and type 2 diabetes mellitus (T2DM) has been repeatedly described in the literature 1, 2, 3, 4. We suggest that the utilization of a diurnal rodent animal model may offer an effective way to further explore metabolic, cardiovascular, and affective-like behavioral changes related to chronodisruption and their underlying mechanisms. ![]() Our results demonstrate that exercising ameliorates pathological-like daily rhythms in activity and blood glucose levels, glucose tolerance and depressive- and anxiety-like behaviors in the sand rat model, supporting the important role of physical activity in modulating the “circadian syndrome” and circadian rhythm-related diseases. Animals with access to a running wheel had larger heart weight and heart/body weight ratio, and thicker left ventricular wall. Voluntary exercise strengthened general activity rhythms, improved memory and lowered anxiety- and depressive-like behaviors, enhanced oral glucose tolerance, and decreased plasma insulin levels and liver weight. We explored the beneficial effects of voluntary wheel running on daily rhythms, and the development of depression, T2DM, and CVD in a diurnal animal model, the fat sand rat ( Psammomys obesus). Physical exercise synchronizes the circadian system and has ameliorating effects on the depression- and anxiety-like phenotype induced by circadian disruption in mice and sand rats. Emerging evidence suggests that disruption of circadian rhythmicity contributes to development of comorbid depression, cardiovascular diseases (CVD), and type 2 diabetes mellitus (T2DM).
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