Mathematical modeling informs the impact of changes in circadian rhythms and meal patterns on insulin secretion

Bae, Seul-A; Androulakis, Ioannis P.

doi:10.1152/ajpregu.00230.2018

Cited by 10 publications

(4 citation statements)

References 42 publications

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“…(vi) The influences of other causes of perturbation and response of the HPA axis (e.g., stress and posture) should be added to the model. (vii) The mathematical model presented in this work can be expanded to explicitly account for the influence of cortisol on the dynamics of metabolic mediators such as glucose and insulin as has been shown by others [ 57 , 60 , 61 , 62 , 63 ]. Such extensions would enable further investigation of the interplay among timing of meals, sleep cycles, and light exposure, which are often perturbed together for extended periods in chronic shift workers.…”

Section: Discussionmentioning

confidence: 99%

Modeling the Influence of Chronic Sleep Restriction on Cortisol Circadian Rhythms, with Implications for Metabolic Disorders

et al. 2021

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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 primary hormone of the HPA axis, exhibits robust circadian rhythmicity and is moderately influenced by sleep and wake states and other physiology. Several studies have explored the effects of acute or chronic sleep deficiency (i.e., usually from self-selected chronic sleep restriction, CSR) on the HPA axis. Quantifying long-term changes in the circadian rhythm of cortisol under CSR in controlled conditions is inadequately studied due to practical limitations. We use a semi-mechanistic mathematical model of the HPA axis and the sleep/wake cycle to explore the influence of CSR on cortisol circadian rhythmicity. In qualitative agreement with experimental findings, model simulations predict that CSR results in physiologically relevant disruptions in the phase and amplitude of the cortisol rhythm. The mathematical model presented in this work provides a mechanistic framework to further explore how CSR might lead to HPA axis disruption and subsequent development of chronic metabolic complications.

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Section: Discussionmentioning

confidence: 99%

Modeling the Influence of Chronic Sleep Restriction on Cortisol Circadian Rhythms, with Implications for Metabolic Disorders

et al. 2021

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“…The model was further expanded in Mavroudis, Corbett, Calvano, and Androulakis (2015) to account for the presence of two receptors: the glucocorticoid (GR) and the mineralocorticoid (MR) which regulate antagonistically the active form of the cortisol/receptor complex. Extensions of these models were later also developed to demonstrate the ability of cortisol's circadian rhythms to entrain peripheral clocks as well as cell cycle dynamics (Mavroudis et al, 2012; Pierre, Rao, Hartmanshenn, & Androulakis, 2018) as well as linking light and metabolic rhythms (Bae & Androulakis, 2017, 2019).…”

Section: Biological Oscillators and The Hpa Axismentioning

confidence: 99%

Circadian rhythms and the HPA axis: A systems view

Androulakis

2021

WIREs Mechanisms of Disease

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The circadian timing system comprises a network of time‐keeping clocks distributed across a living host whose responsibility is to allocate resources and distribute functions temporally to optimize fitness. The molecular structures generating these rhythms have evolved to accommodate the rotation of the earth in an attempt to primarily match the light/dark periods during the 24‐hr day. To maintain synchrony of timing across and within tissues, information from the central clock, located in the suprachiasmatic nucleus, is conveyed using systemic signals. Leading among those signals are endocrine hormones, and while the hypothalamic–pituitary–adrenal axis through the release of glucocorticoids is a major pacesetter. Interestingly, the fundamental units at the molecular and physiological scales that generate local and systemic signals share critical structural properties. These properties enable time‐keeping systems to generate rhythmic signals and allow them to adopt specific properties as they interact with each other and the external environment. The purpose of this review is to provide a broad overview of these structures, discuss their functional characteristics, and describe some of their fundamental properties as these related to health and disease. This article is categorized under: Immune System Diseases > Computational Models Immune System Diseases > Biomedical Engineering

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“…Moreover, HFD feeding for 4 weeks significantly altered the rhythms of fatty acid synthesis rate-limiting enzyme hepatic acetyl-CoA carboxylase (ACACA), REV-ERBα and histone regulator HDAC3 ( 33 ). Studies have shown that insulin fluctuations caused by nutrient supply can “reset” the biological clock of the liver ( 34 ). In insulin-deficient mice, this change was not observed ( 35 ) but injection of insulin reset the rhythmicity of genes.…”

Section: Nutrient Control Of the Circadian Clockmentioning

confidence: 99%

Advances in Unhealthy Nutrition and Circadian Dysregulation in Pathophysiology of NAFLD

Guo

Zheng

Zhang

et al. 2021

Front. Clin. Diabetes Healthc.

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Unhealthy diets and lifestyle result in various metabolic conditions including metabolic syndrome and non-alcoholic fatty liver disease (NAFLD). Much evidence indicates that disruption of circadian rhythms contributes to the development and progression of excessive hepatic fat deposition and inflammation, as well as liver fibrosis, a key characteristic of non-steatohepatitis (NASH) or the advanced form of NAFLD. In this review, we emphasize the importance of nutrition as a critical factor in the regulation of circadian clock in the liver. We also focus on the roles of the rhythms of nutrient intake and the composition of diets in the regulation of circadian clocks in the context of controlling hepatic glucose and fat metabolism. We then summarize the effects of unhealthy nutrition and circadian dysregulation on the development of hepatic steatosis and inflammation. A better understanding of how the interplay among nutrition, circadian rhythms, and dysregulated metabolism result in hepatic steatosis and inflammation can help develop improved preventive and/or therapeutic strategies for managing NAFLD.

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Mathematical modeling informs the impact of changes in circadian rhythms and meal patterns on insulin secretion

Cited by 10 publications

References 42 publications

Modeling the Influence of Chronic Sleep Restriction on Cortisol Circadian Rhythms, with Implications for Metabolic Disorders

Modeling the Influence of Chronic Sleep Restriction on Cortisol Circadian Rhythms, with Implications for Metabolic Disorders

Circadian rhythms and the HPA axis: A systems view

Advances in Unhealthy Nutrition and Circadian Dysregulation in Pathophysiology of NAFLD

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