Present findings show for the first time that the 3111T/C SNP of the CLOCK gene is not associated to human obesity and/or BED, but it seems to predispose obese individuals to a higher BMI.
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.
A series of our recent studies revealed that circadian clock proteins are important for hypofibrinolysis induced by metabolic disorders such as obesity and diabetes.
Previous studies have found associations between single nucleotide polymorphisms in clock genes or downstream hormone receptors such as the leptin receptor (LEPR) or glucocorticoid receptor (NR3C1) and obesity in the healthy population, but this association remains to be examined in patients with schizophrenia treated with antipsychotics.
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.
Our results showed that women carrying the C allele of CLOCK gene had a marginally significant lower risk of overweight/obesity compared with noncarrier-TT-subjects (odds ratio [OR]: .61, 95% confidence interval [CI]: .36-1.04; p = .069).
Single nucleotide polymorphisms (SNPs) of the circadian locomotor output cycles kaput (CLOCK) gene have been associated with cardiometabolic conditions such as obesity and dyslipidemia.
Variant of the CLOCK gene and related haplotypes are associated with the prevalence of T2D in the Japanese population, in which obesity is less common, and the association between CLOCK gene variant at rs1801260 and the prevalence of diabetes is enhanced in normal-weight subjects.
However, little is known about the relationship between circadian preferences and genetic background in CLOCK genes with obesity and weight loss among severely obese patients after bariatric surgery.
These findings suggest that a change in photoperiod can partly disrupt the circadian rhythmcity of clock genes, impair lipid metabolism, and promote obesity.