We provide evidence that voluntary wheel running increases core clock protein abundance and influences diet-induced obesity in mice in a time-of-day-dependent manner.
Adipose tissue dysfunction in obesity has previously been linked to disruption of the intrinsic adipose clock gene network that is crucial for normal metabolic function.
These findings suggest that a change in photoperiod can partly disrupt the circadian rhythmcity of clock genes, impair lipid metabolism, and promote obesity.
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.
Single nucleotide polymorphisms (SNPs) of the circadian locomotor output cycles kaput (CLOCK) gene have been associated with cardiometabolic conditions such as obesity and dyslipidemia.
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).
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.