Abstract:The sleep duration of adolescents has continued to decline over the past 20 years. Sleep insufficiency is one of the most important risk factors for obesity, but the mechanisms underlying the association are unclear. Therefore, the hypothalamic-regulated mechanisms of appetite and the circadian clock gene expression were examined in sleep-restricted rats. Rats aged 7 weeks were randomly divided into two groups: the control group and sleep restriction group (7 rats/group) rats were sleep-restricted for 4 weeks.… Show more
“…Young rats sleep deprived also experienced an alteration of the genes involved in the transcriptional feedback loop regulated by CLOCK and BMAL1 proteins. All these events confirm that alteration of sleep length causes dysregulation of several pathways in the hypothalamus with consequences in the regulation of hunger and energy consumption [ 15 ].…”
Section: Sleep Deprivation Effects In Rat Modelsmentioning
Sleep health and its adaptation to individual and environmental factors are crucial to promote physical and mental well-being across animal species. In recent years, increasing evidence has been reported regarding the relationship between sleep and the immune system and how sleep disturbances may perturb the delicate balance with severe repercussions on health outcomes. For instance, experimental sleep deprivation studies in vivo have reported several major detrimental effects on immune health, including induced failure of host defense in rats and increased risk for metabolic syndrome (MetS) and immune suppression in humans. In addition, two novel risk factors for dysregulated metabolic physiology have recently been identified: sleep disruption and circadian misalignment. In light of these recent findings about the interplay between sleep and the immune system, in this review, we focus on the relationship between sleep deprivation and immunity against viruses, with a special interest in SARS-CoV-2 infection.
“…Young rats sleep deprived also experienced an alteration of the genes involved in the transcriptional feedback loop regulated by CLOCK and BMAL1 proteins. All these events confirm that alteration of sleep length causes dysregulation of several pathways in the hypothalamus with consequences in the regulation of hunger and energy consumption [ 15 ].…”
Section: Sleep Deprivation Effects In Rat Modelsmentioning
Sleep health and its adaptation to individual and environmental factors are crucial to promote physical and mental well-being across animal species. In recent years, increasing evidence has been reported regarding the relationship between sleep and the immune system and how sleep disturbances may perturb the delicate balance with severe repercussions on health outcomes. For instance, experimental sleep deprivation studies in vivo have reported several major detrimental effects on immune health, including induced failure of host defense in rats and increased risk for metabolic syndrome (MetS) and immune suppression in humans. In addition, two novel risk factors for dysregulated metabolic physiology have recently been identified: sleep disruption and circadian misalignment. In light of these recent findings about the interplay between sleep and the immune system, in this review, we focus on the relationship between sleep deprivation and immunity against viruses, with a special interest in SARS-CoV-2 infection.
“…After the 6-week CSD intervention, the bone formation and bone resorption makers were both significantly lower than in the NC group ( P <0.05), suggesting that CSD suppressed bone turnover status of growing rats, mainly affecting bone formation. Since the body weight has been shown to positively correlate with the bone loss, 16 the differences remained significant even after adjustment for covariates, weight. Figure 2 Chronic sleep deprivation (CSD) leaded to bone remodeling imbalance in growing rats.…”
Section: Resultsmentioning
confidence: 95%
“…Xue et al 15 found the expression level of protein p-AKT decreased significantly in the hippocampus with increasing inflammation and oxidative stress after 7 days of SD. Sun et al 16 also reported the reduced expression of IRS/PI3K/AKT/mTOR and FoxO1 signaling pathways in the hypothalamus of 4-week SD rats. Due to PI3K/AKT pathway reduced by SD, some drugs prevent the disorder induced by SD via activating this pathway.…”
Background
This study aimed to assess the effects of chronic sleep deprivation (CSD) on bone metabolism in growing rats and the likely underlying mechanism.
Methods
Twenty 5-week-old male Wistar rats and randomly divided into the CSD and normal control (NC) groups after one-week acclimatization. After a 6-week intervention of sleep deprivation, the distal femurs of both groups were harvested for micro-computed tomography scans and histological analysis. Meanwhile, the femur tissues were measured the mRNA and protein expression via RNA sequencing and immunohistochemical analysis. Serum bone turnover markers were evaluated at 0, 2, 4, and 6 weeks.
Results
CSD impaired the bone growth, showing an imbalance of bone turnover status, dysphasia in the metaphysis growth plate, and deterioration of bone microarchitecture. Further, CSD suppressed bone formation, showing that the expression of osteogenesis-related proteins (col1α1 and osteocalcin) and mRNA (
igf1, bglap, runx2, col1α1, pth1r
) are down-regulated. Differentially expressed genes were detected, and functional enrichment analyses revealed that the PI3K/AKT pathway was significantly down-regulated in the CSD group.
Conclusion
These results suggest that CSD can significantly impaire bone health, and it may exert these effects in part by suppressing bone formation and osteoblast differentiation, and inactivating the PI3K/AKT signaling pathway.
“…In addition to circadian patterns of transcription factors and enzyme expression, the secretion of melatonin, insulin, glucagon, glucagon-like-peptide-1, cortisol, leptin, adiponectin, ghrelin, and RAAS is also coordinated by the molecular clock [ 45 , 46 , 47 , 48 , 49 , 50 , 51 ]. All of these hormones are major regulators of metabolism, and therefore represent an important link between the circadian rhythm and metabolic processes [ 45 , 46 , 47 , 48 , 49 , 50 , 51 ].…”
Section: The Link Between Circadian Clock and Metabolismmentioning
Physiological processes occur in accordance with a rhythm regulated by the endogenous biological clock. This clock is programmed at the molecular level and synchronized with the daily light–dark cycle, as well as activities such as feeding, exercise, and social interactions. It consists of the core clock genes, Circadian Locomotor Output Cycles Protein Kaput (CLOCK) and Brain and Muscle Arnt-Like protein 1 (BMAL1), and their products, the period (PER) and cryptochrome (CRY) proteins, as well as an interlocked feedback loop which includes reverse-strand avian erythroblastic leukemia (ERBA) oncogene receptors (REV-ERBs) and retinoic acid-related orphan receptors (RORs). These genes are involved in the regulation of metabolic pathways and hormone release. Therefore, circadian rhythm disruption leads to development of metabolic syndrome (MetS). MetS refers to a cluster of risk factors (RFs), which are not only associated with the development of cardiovascular (CV) disease (CVD), but also with increased all-cause mortality. In this review, we consider the importance of the circadian rhythm in the regulation of metabolic processes, the significance of circadian misalignment in the pathogenesis of MetS, and the management of MetS in relation to the cellular molecular clock.
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