Novel strategies are required to reduce the risk of developing diabetes and/or clinical outcomes and complications of diabetes. In this regard, the role of the circadian system may be a potential candidate for the prevention of diabetes. We reviewed evidence from animal, clinical, and epidemiological studies linking the circadian system to various aspects of the pathophysiology and clinical outcomes of diabetes. The circadian clock governs genetic, metabolic, hormonal, and behavioral signals in anticipation of cyclic 24-hour events through interactions between a "central clock" in the suprachiasmatic nucleus and "peripheral clocks" in the whole body. Currently, circadian rhythmicity in humans can be subjectively or objectively assessed by measuring melatonin and glucocorticoid levels, core body temperature, peripheral blood, oral mucosa, hair follicles, rest-activity cycles, sleep diaries, and circadian chronotypes. In this review, we summarized various circadian misalignments, such as altered light-dark, sleep-wake, rest-activity, fasting-feeding, shift work, evening chronotype, and social jetlag, as well as mutations in clock genes that could contribute to the development of diabetes and poor glycemic status in patients with diabetes. Targeting critical components of the circadian system could deliver potential candidates for the treatment and prevention of type 2 diabetes mellitus in the future.
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http://dx.doi.org/10.4093/dmj.2023.0193 | DOI Listing |
World J Diabetes
January 2025
National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20810, United States.
Diabetes mellitus (DM) is a debilitating disorder that impacts all systems of the body and has been increasing in prevalence throughout the globe. DM represents a significant clinical challenge to care for individuals and prevent the onset of chronic disability and ultimately death. Underlying cellular mechanisms for the onset and development of DM are multi-factorial in origin and involve pathways associated with the production of reactive oxygen species and the generation of oxidative stress as well as the dysfunction of mitochondrial cellular organelles, programmed cell death, and circadian rhythm impairments.
View Article and Find Full Text PDFJ Comp Physiol A Neuroethol Sens Neural Behav Physiol
January 2025
Graduate School of Science, The University of Osaka, 1-1 Machikaneyama-cho, Toyonaka, Osaka, 560-0043, Japan.
Larvae of the flesh fly, Sarcophaga similis exhibit photoperiodic responses to control pupal diapause. Although the external coincidence model is applicable to S. similis photoperiodism, it remains unknown how the circadian clock system integrates day-length information.
View Article and Find Full Text PDFElife
January 2025
Wellcome Centre for Cell-Matrix Research, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, United Kingdom.
Collagen-I fibrillogenesis is crucial to health and development, where dysregulation is a hallmark of fibroproliferative diseases. Here, we show that collagen-I fibril assembly required a functional endocytic system that recycles collagen-I to assemble new fibrils. Endogenous collagen production was not required for fibrillogenesis if exogenous collagen was available, but the circadian-regulated vacuolar protein sorting (VPS) 33b and collagen-binding integrin α11 subunit were crucial to fibrillogenesis.
View Article and Find Full Text PDFAging Dis
January 2025
Department of Medical Oncology, Shanghai Pulmonary Hospital, School of Medicine, Tongji University, Shanghai, China.
Circadian rhythm is the internal homeostatic physiological clock that regulates the 24-hour sleep/wake cycle. This biological clock helps to adapt to environmental changes such as light, dark, temperature, and behaviors. Aging, on the other hand, is a process of physiological changes that results in a progressive decline in cells, tissues, and other vital systems of the body.
View Article and Find Full Text PDFFASEB J
January 2025
Department of Geriatrics, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
The correct synthesis and degradation of proteins are vital for numerous biological processes in the human body, with protein degradation primarily facilitated by the ubiquitin-proteasome system. The SKP1-CUL1-F-box (SCF) E3 ubiquitin ligase, a member of the Cullin-RING E3 ubiquitin ligase (CRL) family, plays a crucial role in mediating protein ubiquitination and subsequent 26S proteasome degradation during normal cellular metabolism. Notably, SCF is intricately linked to the pathogenesis of various diseases, including malignant tumors.
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