Chronobiology, genetics and metabolic syndrome

Abstract

Circadian rhythms are such an innate part of our lives that we rarely pause to speculate why they even exist. Recently, some studies have suggested that the disruption of the circadian system may be causal for the manifestations of metabolic syndrome (MetS). This review summarizes the latest evidence of the existing interaction among chronobiology, genetics and MetS. Shift work, sleep deprivation and bright light exposure at night are related to increased adiposity and prevalence of MetS. Animal models have revealed that mice with circadian locomotor output cycles kaput (clock) gene disruption are prone to develop a phenotype resembling MetS. Moreover, studies in humans have shown that clock genes are expressed in adipose tissue, and that both their levels of expression and their genetic variants correlate with different components of the MetS. Current studies are illustrating the particular role of different clock gene variants and their predicted haplotypes in MetS. The circadian system has an important impact on metabolic disturbances and vice versa. Although the precise mechanism linking the MetS to chronodisruption is not well known, hypotheses point to the internal desynchronization between different circadian rhythms. The novelty of this area of research is contributing to the development of new and intriguing studies, particularly those focused on the association between different clock genes polymorphisms and MetS traits.