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(A) The circadian drive (green) of the physiological sleep-wake model that regulates the homeostatic drive and the secretion of CRH in a time-of-day dependent manner. (B) The cortisol circadian rhythm (black) given the shown sleep (black shaded bars at top of panels) and light-dark (white and grey shaded regions, respectively) schedules.
Source publication
Chronic sleep deficiency is prevalent in modern society and is associated with increased risk of metabolic and other diseases. While the mechanisms by which chronic sleep deficiency induces pathophysiological changes are yet to be elucidated, the hypothalamic–pituitary–adrenal (HPA) axis may be an important mediator of these effects. Cortisol, the...
Contexts in source publication
Context 1
... the influence of the nominal light schedule, the model parameters are calibrated such that the circadian drive peaks in the middle of the day [35] (Figure 3) and the model of the HPA axis produces a circadian rhythm of cortisol (Figure 3), ACTH, and CRH ( Figure S1). The phase adopted by the cortisol rhythm under the influence of the nominal light schedule and the model generated sleep-schedule closely follows physiological observations [9]. ...
Context 2
... the influence of the nominal light schedule, the model parameters are calibrated such that the circadian drive peaks in the middle of the day [35] (Figure 3) and the model of the HPA axis produces a circadian rhythm of cortisol (Figure 3), ACTH, and CRH ( Figure S1). The phase adopted by the cortisol rhythm under the influence of the nominal light schedule and the model generated sleep-schedule closely follows physiological observations [9]. ...
Context 3
... in contrast, CSR due to an advance in the wake time led to a substantial decrease in the amplitude of the cortisol rhythm, while preserving the phase of the rhythm (Figure 7). The changes in the ACTH rhythm in response to CSR are much less pronounced ( Figure S3) than those of cortisol. ...
Context 4
... difference in the binding affinities of cortisol to these receptors [84] was modeled by setting the Michaelis constant of the mineralocorticoid receptor (KMR) to a lower value than that of glucocorticoid receptor (KGR). Model parameters for the HPA axis (Equations (9)- (11)) were selected such that HPA axis rhythm in the absence of the entraining effects of light adopts a period of slightly greater than 24 h (24.1-24.5 h) [85], while, in the presence of the nominal light schedule, cortisol adopts a robust rhythm with a peak around the beginning of the wake state in qualitative agreement with experimental observations ( Figure S3). Equations (12)- (21) were parameterized based on a corticosteroid pharmacodynamic model calibrated to experimental data on corticosterone and corticosteroid receptor dynamics after methylprednisolone administration [82,86]. ...
Citations
... In turn, cortisol exerts a feedback reaction and causes ACTH and CRH synthesis. In addition, there is a binding affinity of glucocorticoids GRs and mineralocorticoids MRs localized in different brain regions (e.g., hippocampus, amygdala, hypothalamus, and pituitary) [3]. Endocrine action in stress are due to the action of the functional mass of the corticotropes and of the functional mass of the adrenal cells that secrete cortisol using the cell-mass production rates and cell-mass removal rates [4]. ...
... However, these patterns change with short sleep duration (both habitual and experimental) as sleep restriction causes elevated markers of sympathetic activation and catecholamines (49). As a result, cortisol levels become higher in the evening (50) and display a lower rate of decline (51). Such changes can lead to a lower response of b-cells to glucose and reduce insulin sensitivity (driven by lower glucagon-like peptide 1 levels) (52). ...
... morning types) (34) Sleep variability -the daily variation around the mean (i.e. standard deviation) of: time of going to sleep and waking up and midpoint of sleep. Sleep variability is higher in those living with type 2 diabetes and HbA1c concentrations are up to 1% higher among those with the greatest variability (45) weeknights versus the midpoint on weekends) Those with social jet lag of >90 minutes have higher HbA1c levels than those with no social jet lag (51 [44][45][46][47][48][49][50][51][52][53][54][55][56][57][58] vs. 62 [52][53][54][55][56][57][58][59][60][61][62][63][64][65][66][67][68][69][70][71] mmol/mol) (44) ...
For the first time, the latest American Diabetes Association/European Association for the Study of Diabetes (ADA/EASD) consensus guidelines have incorporated a growing body of evidence linking health outcomes associated with type 2 diabetes to the movement behavior composition over the whole 24-h day. Of particular note, the importance of sleep as a key lifestyle component in the management of type 2 diabetes is promulgated and presented using three key constructs: quantity, quality, and timing (i.e., chronotype). In this narrative review we highlight some of the key evidence justifying the inclusion of sleep in the latest consensus guidelines by examining the associations of quantity, quality, and timing of sleep with measures of glycemia, cardiovascular disease risk, and mortality. We also consider potential mechanisms implicated in the association between sleep and type 2 diabetes and provide practical advice for health care professionals about initiating conversations pertaining to sleep in clinical care. In particular, we emphasize the importance of measuring sleep in a free-living environment and provide a summary of the different methodologies and targets. In summary, although the latest ADA/EASD consensus report highlights sleep as a central component in the management of type 2 diabetes, placing it, for the first time, on a level playing field with other lifestyle behaviors (e.g., physical activity and diet), the evidence base for improving sleep (beyond sleep disorders) in those living with type 2 diabetes is limited. This review should act as a timely reminder to incorporate sleep into clinical consultations, ongoing diabetes education, and future interventions.
... Cortisol first binds to high affinity receptors and then to low affinity receptors. Mineralocorticoid receptors are dominant at night and during the day (Rao et al. 2021). ...
Sleep is a globally observable fact, or period of reversible distracted rest, that can be distinguished from arousal by various behavioral criteria. Although the function of sleep is an evolutionarily conserved behavior, its mechanism is not yet clear. The zebrafish (Danio rerio) has become a valuable model for neurobehavioral studies such as studying learning, memory, anxiety, and depression. It is characterized by a sleep-like state and circadian rhythm, making it comparable to mammals. Zebrafish are a good model for behavioral studies because they share genetic similarities with humans. A number of neurotransmitters are involved in sleep and wakefulness. There is a binding between melatonin and the hypocretin system present in zebrafish. The full understanding of sleep and wakefulness physiology in zebrafish is still unclear among researchers. Therefore, to make a clear understanding of the sleep/wake cycle in zebrafish, this article covers the mechanism involved behind it, and the role of the neuromodulator system followed by the mechanism of the HPA axis.
... Although, based on a systematic review and meta-analysis study, it was found that short and long-term sleep duration contributed to the development of type 2 diabetes (43). Restriction of sleep reduces insulin sensitivity the next day by increasing cortisol levels in the nighttime (45,46). In contrast, some infection markers such as IL-6, and C-reactive protein increase in people who report prolonged sleep, which accelerates the progression of diabetes and its complications (47,48). ...
Propose
The present study has sought to investigate the prevalence of diabetes and its related risk factors, to examine the relationship between demographic variables, anthropometric indices, sleep quality, and Metabolic Equivalent Task (MET) with diabetes in Khuzestan province, southwest Iran.
Methods
The present study has a cross-sectional design (the baseline data of the Hoveyzeh cohort study as a sub-branch of the Persian Prospective Cohort Study). Comprehensive information from 10,009 adults (aged 35–70 years) was collected from May 2016 to August 2018 through a multi-part general questionnaire containing general characteristics, marital status, education, smoking, sleep quality, MET, and anthropometric indices. Data analysis was performed by SPSS software version 19.
Results
The mean age of the sample was 52.97 ± 8.99 years. 60.3% of the population were women and 67.7% were illiterate. Out of the 10,009 people surveyed, 1,733 stated that they have diabetes (17%). In 1,711 patients (17%) the amount of FBS was ≥126 mg/dl. There is a statistically significant relationship between diabetes and MET. More than 40% had BMI above 30. Anthropometric indices in diabetic and non-diabetic individuals were different. Also, there was a statistically significant difference between the mean duration of sleep and the use of sleeping pills in diabetic and non-diabetic groups (p < 0.05). Based on logistic regression, marital status [OR = 1.69 (95% CI, 1.24, 2.30)], education level [OR = 1.49 (95% CI, 1.22, 1.83)], MET [OR = 2.30 (95% CI, 2.01, 2.63)], height [OR = 0.99 (95% CI, 0.98, 0.99)], weight [OR = 1.007 (95% CI, 1.006, 1.012)], wrist circumference [OR = 1.10 (95% CI, 1.06, 1.14)], waist circumference [OR = 1.03 (95% CI, 1.02, 1.03)], waist-to-hip ratio [OR = 3.41 (95% CI, 2.70, 4.29)], and BMI [OR = 2.55 (95% CI, 1.53, 4.25)], are good predictors for diabetes.
Conclusion
The results of this study showed that the prevalence of diabetes in Hoveyzeh city, Khuzestan, Iran, was almost high. and emphasize that preventive interventions should focus on risk factors, especially socioeconomic status, and anthropometric indicators along with lifestyle.
... This paradigm may partially explain that hypercortisolism is associated with increased adiposity in Cushing syndrome and paradoxically with decreased adiposity in states of undernutrition, such as anorexia and acute illness. Hypothalamic-pituitary-adrenal (HPA) axis dysfunction, as well as local metabolism of glucocorticoids in adipose tissue, can cause alterations of circulating cortisol dynamics, which have been linked to obesity and the metabolic syndrome [66]. Obese individuals show markedly higher ACTH, and cortisol may respond to vasopressin (AVP) and corticotropin-releasing hormone (CRH) [67,68], whereas dose-response ACTH stimulation test may interfere to elevated cortisol level [69]. ...
Background
The global prevalence of obesity has soared to a concerning height in the past few decades. Interestingly, the global decline in semen quality is a parallel occurrence that urges researchers to evaluate if obesity is among the most essential causatives of male infertility or subfertility.
Main body
Obesity may alter the synchronized working of the reproductive-endocrine milieu, mainly the hypothalamic-pituitary-gonadal (HPG) axis along with its crosstalks with other reproductive hormones. Obesity-mediated impairment in semen parameters may include several intermediate factors, which include physical factors, essentially increased scrotal temperature due to heavy adipose tissue deposits, and systemic inflammation and oxidative stress (OS) initiated by various adipose tissue-derived pro-inflammatory mediators. Obesity, via its multifaceted mechanisms, may modulate sperm genetic and epigenetic conformation, which severely disrupt sperm functions. Paternal obesity reportedly has significant adverse effects upon the outcome of assisted reproductive techniques (ARTs) and the overall health of offspring. Given the complexity of the underlying mechanisms and rapid emergence of new evidence-based hypotheses, the concept of obesity-mediated male infertility needs timely updates and pristine understanding.
Conclusions
The present review comprehensively explains the possible obesity-mediated mechanisms, especially via physical factors, OS induction, endocrine modulation, immune alterations, and genetic and epigenetic changes, which may culminate in perturbed spermatogenesis, disrupted sperm DNA integrity, compromised sperm functions, and diminished semen quality, leading to impaired male reproductive functions.
... Bae & Androulakis [56,57] developed models to study the impact of the circadian clock on insulin secretion and gluconeogenesis, showing how external signals (light/dark cycles and feeding/fasting cycles) affect metabolism over the course of a day. In a different vein, Rao et al. [58] used a model of the hypothalamus--pituitaryadrenal axis and the sleep/wake cycle to explore the influence of sleep deficiency on daily rhythms of cortisol release. ...
To survive and reproduce, a cell must process information from its environment and its own internal state and respond accordingly, in terms of metabolic activity, gene expression, movement, growth, division and differentiation. These signal–response decisions are made by complex networks of interacting genes and proteins, which function as biochemical switches and clocks, and other recognizable information-processing circuitry. This theme issue of Interface Focus (in two parts) brings together articles on time-keeping and decision-making in living cells—work that uses precise mathematical modelling of underlying molecular regulatory networks to understand important features of cell physiology. Part I focuses on time-keeping: mechanisms and dynamics of biological oscillators and modes of synchronization and entrainment of oscillators, with special attention to circadian clocks.
... Most people cannot reach the recommended sleep time [1,2]. Lack of sleep causes extensive harm to human health, including metabolic function, emotional regulation, and adverse effects on cognitive function [3][4][5][6]. Sleep regulation includes sleep pressure (process S) and the circadian rhythm (process C). As waking time increases, sleep pressure increases, leading to sleep. ...
Lack of sleep time is a menace to modern people, and it leads to chronic diseases and mental illnesses. Circadian processes control sleep, but little is known about how sleep affects the circadian system. Therefore, we performed a 28-day sleep restriction (SR) treatment in mice. Sleep restriction disrupted the clock genes’ circadian rhythm. The circadian rhythms of the Cry1 and Per1/2/3 genes disappeared. The acrophase of the clock genes (Bmal1, Clock, Rev-erbα, and Rorβ) that still had a circadian rhythm was advanced, while the acrophase of negative clock gene Cry2 was delayed. Clock genes’ upstream signals ERK and EIFs also had circadian rhythm disorders. Accompanied by changes in the central oscillator, the plasma output signal (melatonin, corticosterone, IL-6, and TNF-α) had an advanced acrophase. While the melatonin mesor was decreased, the corticosterone, IL-6, and TNF-α mesor was increased. Our results indicated that chronic sleep loss could disrupt the circadian rhythm of the central clock through ERK and EIFs and affect the output signal downstream of the core biological clock.
Aging causes progressive deterioration of daily rhythms in behavioral and metabolic processes and disruption in the regular sleep-wake cycle. Circadian disruption is directly related to diverse age-induced health abnormalities. Rising evidence from various organisms shows that core clock gene mutations cause premature aging, reduced lifespan, and sleeping irregularities. Improving the clock functions and correcting its disruption by pharmacological interventions or time-regulated feeding patterns could be a novel avenue for effective clinical management of aging and sleep disorders. To this end, many drugs for sleep disorders and anti-aging compounds interact with the core clock machinery and alter the circadian output. Evaluation of dosing time-dependency and circadian regulation of drug metabolism for therapeutic improvement of the existing drugs is another fundamental facet of chronomedine. Multiple studies have demonstrated dose-dependent manipulation of the circadian period and phase-shifting by pharmacologically active compounds. The chronobiology research field is gradually moving towards the development of novel therapeutic strategies based on targeting the molecular clock or dosing time-oriented medications. However, such translational research ventures would require more experimental evidence from studies on humans. This review discusses the impact of circadian rhythms on aging and sleep, emphasizing the potentiality of circadian medicine in aging attenuation and sleep disorders.
Diet and nutrition play a fundamental role not only in human body composition and in physiology, but have also relevant effects on mood, mental well-being and cognitive performance. In particular, the preservation of mental well-being through a healthy lifestyle, including a well-balanced diet and, in case, through the intake of specific food supplements, is of particular relevance in the perspective of global human ageing, as the brain is affected significantly by a persistent presence of stress factors. Due to the increasing burden of mental and neurological disorders and to the universality of food as a modifiable risk factor, even limited improvements in nutritional habits may translate to a considerable rise of well-being and mental health in the global population. Moreover, the use of targeted, well-balanced food supplements aiming to support the mental health and well-being will probably represent a relevant tool in future decades, together with an increased awareness of the importance of nutrition, also considering the COVID-19 pandemic and the related stressful events and limitations we are still experiencing at global level. The aim of this review is to summarize the experimental and clinical data reported in the literature concerning the beneficial effects of a subset of micro- and macronutrients contained both in food and in supplements, namely magnesium, folic acid, docosahexaenoic acid, eicosapentaenoic acid, and alpha-tocopherol, on a series of disorders, including stress, anxiety, low sleep quality, and low cognitive performance.
Global rates of obesity and Type 2 diabetes mellitus (T2DM) are increasing globally concomitant with a rising prevalence of sleep deprivation and sleep disorders. Understanding the links between sleep, obesity and T2DM might offer an opportunity to develop better prevention and treatment strategies for these epidemics. Experimental studies have shown that sleep restriction is associated with changes in energy homeostasis, insulin resistance and β-cell function. Epidemiological cohort studies established short sleep duration as a risk factor for developing obesity and T2DM. In addition, small studies suggested that short sleep duration was associated less weight loss following lifestyle interventions or bariatric surgery. In this article, we review the epidemiological evidence linking sleep duration to obesity and T2DM and plausible mechanisms. In addition, we review the impact of changes in sleep duration on obesity and T2DM.
