scholarly journals The Association between Circadian Clock Gene Polymorphisms and Metabolic Syndrome: A Systematic Review and Meta-Analysis

Biology ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 20
Author(s):  
Ivana Škrlec ◽  
Jasminka Talapko ◽  
Snježana Džijan ◽  
Vera Cesar ◽  
Nikolina Lazić ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Circadian Rhythm ◽  
Circadian Clock ◽  
Gene Polymorphisms ◽  
Clock Gene ◽  
Meta Analysis ◽  
Predictive Biomarkers ◽  
Circadian Clock Gene ◽  
Increased Risk ◽  
Research Findings

Metabolic syndrome (MetS) is a combination of cardiovascular risk factors associated with type 2 diabetes, obesity, and cardiovascular diseases. The circadian clock gene polymorphisms are very likely to participate in metabolic syndrome genesis and development. However, research findings of the association between circadian rhythm gene polymorphisms and MetS and its comorbidities are not consistent. In this study, a review of the association of circadian clock gene polymorphisms with overall MetS risk was performed. In addition, a meta-analysis was performed to clarify the association between circadian clock gene polymorphisms and MetS susceptibility based on available data. The PubMed and Scopus databases were searched for studies reporting the association between circadian rhythm gene polymorphisms (ARNTL, BMAL1, CLOCK, CRY, PER, NPAS2, REV-ERBα, REV-ERBβ, and RORα) and MetS, and its comorbidities diabetes, obesity, and hypertension. Thirteen independent studies were analyzed with 17,381 subjects in total. The results revealed that the BMAL1 rs7950226 polymorphism was associated with an increased risk of MetS in the overall population. In contrast, the CLOCK rs1801260 and rs6850524 polymorphisms were not associated with MetS. This study suggests that some circadian rhythm gene polymorphisms might be associated with MetS in different populations and potentially used as predictive biomarkers for MetS.

scholarly journals Breast cancer risk, nightwork, and circadian clock gene polymorphisms

2014 ◽  
Vol 21 (4) ◽  
pp. 629-638 ◽  
Author(s):  
Thérèse Truong ◽  
Benoît Liquet ◽  
Florence Menegaux ◽  
Sabine Plancoulaine ◽  
Pierre Laurent-Puig ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Circadian Clock ◽  
Postmenopausal Women ◽  
Gene Polymorphisms ◽  
Clock Gene ◽  
Gene Variants ◽  
Circadian Clock Gene

Night shift work has been associated with an increased risk of breast cancer pointing to a role of circadian disruption. We investigated the role of circadian clock gene polymorphisms and their interaction with nightwork in breast cancer risk in a population-based case–control study in France including 1126 breast cancer cases and 1174 controls. We estimated breast cancer risk associated with each of the 577 single nucleotide polymorphisms (SNPs) in 23 circadian clock genes. We also used a gene- and pathway-based approach to investigate the overall effect on breast cancer of circadian clock gene variants that might not be detected in analyses based on individual SNPs. Interactions with nightwork were tested at the SNP, gene, and pathway levels. We found that two SNPs inRORA(rs1482057 and rs12914272) were associated with breast cancer in the whole sample and among postmenopausal women. In this subpopulation, we also reported an association with rs11932595 inCLOCK, and withCLOCK,RORA, andNPAS2in the analyses at the gene level. Breast cancer risk in postmenopausal women was also associated with overall genetic variation in the circadian gene pathway (P=0.04), but this association was not detected in premenopausal women. There was some evidence of an interaction betweenPER1and nightwork in breast cancer in the whole sample (P=0.024), although the effect was not statistically significant after correcting for multiple testing (P=0.452). Our results support the hypothesis that circadian clock gene variants modulate breast cancer risk.

scholarly journals Circadian Clock Gene Polymorphisms and Sleep-Onset Problems in a Population-Based Cohort Study: The Yamagata Study

2021 ◽  
Vol 255 (4) ◽  
pp. 325-331
Author(s):  
Kaori Sakurada ◽  
Tsuneo Konta ◽  
Sanae Takahashi ◽  
Narumi Murakami ◽  
Hidenori Sato ◽  
...  
Keyword(s):  
Cohort Study ◽  
Circadian Clock ◽  
Gene Polymorphisms ◽  
Clock Gene ◽  
Sleep Onset ◽  
Population Based ◽  
Circadian Clock Gene

scholarly journals RNAi of the circadian clock gene period disrupts the circadian rhythm but not the circatidal rhythm in the mangrove cricket

2012 ◽  
Vol 8 (4) ◽  
pp. 488-491 ◽  
Author(s):  
Hiroki Takekata ◽  
Yu Matsuura ◽  
Shin G. Goto ◽  
Aya Satoh ◽  
Hideharu Numata
Keyword(s):  
Circadian Rhythm ◽  
Circadian Clock ◽  
Molecular Basis ◽  
Clock Gene ◽  
Circadian Clock Gene ◽  
Double Stranded Rna ◽  
Activity Intensity ◽  
Significant Difference ◽  
Clock Mechanism

The clock mechanism for circatidal rhythm has long been controversial, and its molecular basis is completely unknown. The mangrove cricket, Apteronemobius asahinai , shows two rhythms simultaneously in its locomotor activity: a circatidal rhythm producing active and inactive phases as well as a circadian rhythm modifying the activity intensity of circatidal active phases. The role of the clock gene period ( per ), one of the key components of the circadian clock in insects, was investigated in the circadian and circatidal rhythms of A. asahinai using RNAi. After injection of double-stranded RNA of per , most crickets did not show the circadian modulation of activity but the circatidal rhythm persisted without a significant difference in the period from controls. Thus, per is functionally involved in the circadian rhythm but plays no role, or a less important role, in the circatidal rhythm. We conclude that the circatidal rhythm in A. asahinai is controlled by a circatidal clock whose molecular mechanism is different from that of the circadian clock.

scholarly journals Circadian Clock Gene Polymorphisms and Sleep–Wake Disturbance in Alzheimer Disease

2011 ◽  
Vol 19 (7) ◽  
pp. 635-643 ◽  
Author(s):  
Jerome A. Yesavage ◽  
Art Noda ◽  
Beatriz Hernandez ◽  
Leah Friedman ◽  
Jauhtai J. Cheng ◽  
...  
Keyword(s):  
Alzheimer Disease ◽  
Circadian Clock ◽  
Gene Polymorphisms ◽  
Clock Gene ◽  
Circadian Clock Gene

scholarly journals Circadian Clock Gene Polymorphisms in Alcohol Use Disorders and Alcohol Consumption

2010 ◽  
Vol 45 (4) ◽  
pp. 303-311 ◽  
Author(s):  
L. Kovanen ◽  
S. T. Saarikoski ◽  
J. Haukka ◽  
S. Pirkola ◽  
A. Aromaa ◽  
...  
Keyword(s):  
Alcohol Consumption ◽  
Alcohol Use ◽  
Circadian Clock ◽  
Gene Polymorphisms ◽  
Clock Gene ◽  
Alcohol Use Disorders ◽  
Circadian Clock Gene

scholarly journals Cognitive Impairment and Dementia: Gaining Insight through Circadian Clock Gene Pathways

Biomolecules ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 1002
Author(s):  
Kenneth Maiese
Keyword(s):  
Circadian Rhythm ◽  
Cognitive Impairment ◽  
Circadian Clock ◽  
Neurodegenerative Disorders ◽  
Clock Gene ◽  
Clock Genes ◽  
Financial Burden ◽  
Motor Deficits ◽  
Circadian Clock Gene ◽  
Age Related

Neurodegenerative disorders affect fifteen percent of the world’s population and pose a significant financial burden to all nations. Cognitive impairment is the seventh leading cause of death throughout the globe. Given the enormous challenges to treat cognitive disorders, such as Alzheimer’s disease, and the inability to markedly limit disease progression, circadian clock gene pathways offer an exciting strategy to address cognitive loss. Alterations in circadian clock genes can result in age-related motor deficits, affect treatment regimens with neurodegenerative disorders, and lead to the onset and progression of dementia. Interestingly, circadian pathways hold an intricate relationship with autophagy, the mechanistic target of rapamycin (mTOR), the silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) (SIRT1), mammalian forkhead transcription factors (FoxOs), and the trophic factor erythropoietin. Autophagy induction is necessary to maintain circadian rhythm homeostasis and limit cortical neurodegenerative disease, but requires a fine balance in biological activity to foster proper circadian clock gene regulation that is intimately dependent upon mTOR, SIRT1, FoxOs, and growth factor expression. Circadian rhythm mechanisms offer innovative prospects for the development of new avenues to comprehend the underlying mechanisms of cognitive loss and forge ahead with new therapeutics for dementia that can offer effective clinical treatments.

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