Adipose tissue, adipocytes and the circadian timing system

Abstract

Circadian clocks time the daily occurrence of multiple aspects of behaviour and physiology. Through studies of chronic misalignment between our internal clocks and the environment (e.g. during shift work), it has long been postulated that disruption of circadian rhythms is detrimental to human health. Recent advances in understanding of the cellular and molecular basis of mammalian circadian timing mechanisms have identified many key genes involved in circadian rhythm generation and demonstrated the presence of clocks throughout the body. Furthermore, clear links between sleep, circadian rhythms and metabolic function have been revealed and much current research is studying these links in more detail. Here, we review the current evidence linking circadian rhythms, clock genes and adipose biology. We also highlight gaps in our understanding and finally suggest avenues for future research.

Sleep Duration and Adolescent Obesity

“…This could affect the central clock, which in turn could affect the peripheral clock in adipose tissue, leading to abnormal timing of adipocyte differentiation and the release of adipokines. 32,33 In support, a cross-sectional study observed that adolescents going to bed late tended to have higher BMIs, independent of sleep duration, compared with adolescents who go to bed early. 34 To test if this circadian rhythm hypothesis explains the relationship between sleep duration and adolescent weight, future studies could specifically control for evening electronic screen exposure, and evening food intake; and investigate if variants in clock genes (eg, CLOCK and BAML1) modify the association between sleep duration and adolescent BMI.…”

“…32,33 Adolescents with short sleep may be more likely to be awake at night and be exposed to light during the dark cycle. This could affect the central clock, which in turn could affect the peripheral clock in adipose tissue, leading to abnormal timing of adipocyte differentiation and the release of adipokines.…”

Sleep Duration and Overweight/Obesity in Preschool-Aged Children: A Prospective Study of up to 48,922 Children of the Jiaxing Birth Cohort

“…24 In addition, short sleep duration was found to be associated with reduced leptin and elevated ghrelin, which may increase hunger and appetite, contributing to an increased BMI. 22,25 Short sleep may also disrupt circadian rhythms, leading to abnormal timing of adipocyte differentiation and release of adipokines, 26 which were reported in obese human subjects. 27 The mechanism behind the association between prolonged sleep duration and overweight/obesity is not clear.…”

Modulation of Clock Gene Expression by the Transcriptional Coregulator Receptor Interacting Protein 140 (RIP140)

“…In the liver, it regulates lipid and glucose homeostasis, acting either as a corepressor or as a coactivator, depending on the target gene (Herzog et al, 2007). Mounting evidence shows that the maintenance of circadian rhythms is essential to sustain a normal metabolic status (Eckel-Mahan and Sassone-Corsi, 2009; Froy, 2010; Johnston et al, 2009; Kohsaka and Bass, 2007) and that an intact circadian clock in the liver is required to maintain systemic glucose homeostasis (Lamia et al, 2008). Here, we show that the metabolic regulator RIP140, while it is not essential for the maintenance of circadian rhythmicity in cells, modulates clock gene expression by potentiating the activity of ROR nuclear receptors.…”