Sleep and Circadian Rhythm Disturbances in Diabetes: A Narrative Review

Rutters, Femke; Nefs, Giesje

doi:10.2147/dmso.s354026

Cited by 14 publications

(6 citation statements)

References 92 publications

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“…173 Studies investigating pharmacological interventions, such as benzodiazepines and orexin receptor antagonists on glucose metabolism have demonstrated inconclusive results. 171,174…”

Section: Commonly Utilized Sleep Interventions Include Sleep Extensio...mentioning

confidence: 99%

“…In an open‐label randomized‐controlled trial investigating effects of sleep education in patients with prediabetes and type 2 diabetes mellitus, education on the importance of sleep and timing of sleep improved sleep quality, fasting glucose and HbA1c levels in the short term (3 months), although 6 months postintervention, the reduction of fasting glucose was no longer apparent 173 . Studies investigating pharmacological interventions, such as benzodiazepines and orexin receptor antagonists on glucose metabolism have demonstrated inconclusive results 171,174 …”

Section: Restoration Of Circadian Synchronymentioning

confidence: 99%

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Circadian desynchrony and glucose metabolism

Speksnijder,

Bisschop,

Siegelaar

et al. 2024

Journal of Pineal Research

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The circadian timing system controls glucose metabolism in a time‐of‐day dependent manner. In mammals, the circadian timing system consists of the main central clock in the bilateral suprachiasmatic nucleus (SCN) of the anterior hypothalamus and subordinate clocks in peripheral tissues. The oscillations produced by these different clocks with a period of approximately 24‐h are generated by the transcriptional‐translational feedback loops of a set of core clock genes. Glucose homeostasis is one of the daily rhythms controlled by this circadian timing system. The central pacemaker in the SCN controls glucose homeostasis through its neural projections to hypothalamic hubs that are in control of feeding behavior and energy metabolism. Using hormones such as adrenal glucocorticoids and melatonin and the autonomic nervous system, the SCN modulates critical processes such as glucose production and insulin sensitivity. Peripheral clocks in tissues, such as the liver, muscle, and adipose tissue serve to enhance and sustain these SCN signals. In the optimal situation all these clocks are synchronized and aligned with behavior and the environmental light/dark cycle. A negative impact on glucose metabolism becomes apparent when the internal timing system becomes disturbed, also known as circadian desynchrony or circadian misalignment. Circadian desynchrony may occur at several levels, as the mistiming of light exposure or sleep will especially affect the central clock, whereas mistiming of food intake or physical activity will especially involve the peripheral clocks. In this review, we will summarize the literature investigating the impact of circadian desynchrony on glucose metabolism and how it may result in the development of insulin resistance. In addition, we will discuss potential strategies aimed at reinstating circadian synchrony to improve insulin sensitivity and contribute to the prevention of type 2 diabetes.

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“…173 Studies investigating pharmacological interventions, such as benzodiazepines and orexin receptor antagonists on glucose metabolism have demonstrated inconclusive results. 171,174…”

Section: Commonly Utilized Sleep Interventions Include Sleep Extensio...mentioning

confidence: 99%

Section: Restoration Of Circadian Synchronymentioning

confidence: 99%

Circadian desynchrony and glucose metabolism

Speksnijder,

Bisschop,

Siegelaar

et al. 2024

Journal of Pineal Research

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“…These changes can be reversed by melatonin [ 57 , 58 ], highlighting the importance of pineal melatonin in the circadian optimization of pancreatic β-cell function. Circadian dysregulation is also intimately linked to a diverse array of T1DM symptomatology [ 59 ], including nocturnal non-dipping blood pressure increasing kidney disease [ 60 ], cardiac autonomic neuropathy [ 61 ], platelet morphology [ 62 ], microvascular complications [ 63 ], and patterned immune activity [ 64 ], whilst circadian variation in basal insulin requirement can be an early marker of autoimmune polyendocrine syndromes in T1DM [ 65 ]. Such data highlight the role of alterations in the circadian rhythm in T1DM pathophysiology.…”

Section: Wider T1dm Pathophysiologymentioning

confidence: 99%

Type I Diabetes Pathoetiology and Pathophysiology: Roles of the Gut Microbiome, Pancreatic Cellular Interactions, and the ‘Bystander’ Activation of Memory CD8+ T Cells

Anderson¹

2023

IJMS

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Type 1 diabetes mellitus (T1DM) arises from the failure of pancreatic β-cells to produce adequate insulin, usually as a consequence of extensive pancreatic β-cell destruction. T1DM is classed as an immune-mediated condition. However, the processes that drive pancreatic β-cell apoptosis remain to be determined, resulting in a failure to prevent ongoing cellular destruction. Alteration in mitochondrial function is clearly the major pathophysiological process underpinning pancreatic β-cell loss in T1DM. As with many medical conditions, there is a growing interest in T1DM as to the role of the gut microbiome, including the interactions of gut bacteria with Candida albicans fungal infection. Gut dysbiosis and gut permeability are intimately associated with raised levels of circulating lipopolysaccharide and suppressed butyrate levels, which can act to dysregulate immune responses and systemic mitochondrial function. This manuscript reviews broad bodies of data on T1DM pathophysiology, highlighting the importance of alterations in the mitochondrial melatonergic pathway of pancreatic β-cells in driving mitochondrial dysfunction. The suppression of mitochondrial melatonin makes pancreatic β-cells susceptible to oxidative stress and dysfunctional mitophagy, partly mediated by the loss of melatonin’s induction of PTEN-induced kinase 1 (PINK1), thereby suppressing mitophagy and increasing autoimmune associated major histocompatibility complex (MHC)-1. The immediate precursor to melatonin, N-acetylserotonin (NAS), is a brain-derived neurotrophic factor (BDNF) mimic, via the activation of the BDNF receptor, TrkB. As both the full-length and truncated TrkB play powerful roles in pancreatic β-cell function and survival, NAS is another important aspect of the melatonergic pathway relevant to pancreatic β-cell destruction in T1DM. The incorporation of the mitochondrial melatonergic pathway in T1DM pathophysiology integrates wide bodies of previously disparate data on pancreatic intercellular processes. The suppression of Akkermansia muciniphila, Lactobacillus johnsonii, butyrate, and the shikimate pathway—including by bacteriophages—contributes to not only pancreatic β-cell apoptosis, but also to the bystander activation of CD8+ T cells, which increases their effector function and prevents their deselection in the thymus. The gut microbiome is therefore a significant determinant of the mitochondrial dysfunction driving pancreatic β-cell loss as well as ‘autoimmune’ effects derived from cytotoxic CD8+ T cells. This has significant future research and treatment implications.

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“…The complications of CKD intensify insomnia as well as depression, anxiety, and itch, which often affect patients with decreased kidney function [ 73 , 74 , 75 ]. A chronic deficit of sleep can lead to metabolic and endocrine disorders, e.g., diabetes, obesity, or hypertension [ 76 , 77 , 78 , 79 , 80 , 81 ]. Behavioral interventions and pharmacological treatments are often not sufficient [ 82 ].…”

Section: The Role Of Melatonin In Kidney Diseasesmentioning

confidence: 99%

Melatonin Treatment in Kidney Diseases

Markowska

Niemczyk

Romejko

2023

Cells

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Melatonin is a neurohormone that is mainly secreted by the pineal gland. It coordinates the work of the superior biological clock and consequently affects many processes in the human body. Disorders of the waking and sleeping period result in nervous system imbalance and generate metabolic and endocrine derangements. The purpose of this review is to provide information regarding the potential benefits of melatonin use, particularly in kidney diseases. The impact on the cardiovascular system, diabetes, and homeostasis causes melatonin to be indirectly connected to kidney function and quality of life in people with chronic kidney disease. Moreover, there are numerous reports showing that melatonin plays a role as an antioxidant, free radical scavenger, and cytoprotective agent. This means that the supplementation of melatonin can be helpful in almost every type of kidney injury because inflammation, apoptosis, and oxidative stress occur, regardless of the mechanism. The administration of melatonin has a renoprotective effect and inhibits the progression of complications connected to renal failure. It is very important that exogenous melatonin supplementation is well tolerated and that the number of side effects caused by this type of treatment is low.

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Sleep and Circadian Rhythm Disturbances in Diabetes: A Narrative Review

Cited by 14 publications

References 92 publications

Circadian desynchrony and glucose metabolism

Circadian desynchrony and glucose metabolism

Type I Diabetes Pathoetiology and Pathophysiology: Roles of the Gut Microbiome, Pancreatic Cellular Interactions, and the ‘Bystander’ Activation of Memory CD8+ T Cells

Melatonin Treatment in Kidney Diseases

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