Metabolic homeostasis is linked to the circadian clock (rhythm), with multiple signaling pathways in organs regulated by circadian clock genes, and recent studies of circadian clock gene functions suggest that disruption of the circadian rhythm is associated with significant morbidity and mortality, including the metabolic syndrome.
Our data showed a nominal association of MetS with several single nucleotide polymorphisms (SNPs) in five key circadian clock genes including ARNTL, GSK3B, PER3, RORA, and RORB; but none of these SNPs persisted significantly after performing Bonferroni correction.
Our data support the notion that a chronic consumption of a healthy diet may play a contributing role in triggering glucose metabolism by interacting with the rs1801260 SNP at CLOCK gene locus in MetS patients.
The aim of this research was to investigate the influence of obesity and metabolic syndrome (MetS) features in clock gene methylation and the involvement of these epigenetic modifications in the outcomes.
Thus, the aim of the present study was to determine whether the development of menopause induces an alteration of the genes that control biological rhythms in human subcutaneous (SAT) and visceral (VAT) adipose tissue, and whether changes in clock gene expression are involved in the increased risk of developing metabolic syndrome (MetS), which is frequently associated with menopause.
A significant interaction between the 5-HTTLPR variant and the haplotype rs1554483-rs4864548 of the CLOCK gene was detected for diastolic (p = .0058) and systolic blood pressure (p = .0014), arterial hypertension (p = .033), plasma triglycerides levels (p = .033), and number of MS components (p = .01).
These findings suggest that the Clock gene CGC haplotype may be protective for the development of obesity and support the hypothesis that genetic variation in the Clock gene may play a role in the development of the metabolic syndrome, type 2 diabetes and cardiovascular disease.