bims-ciryme 2023-08-06 papers

Issue of 2023‒08‒06
two papers selected by
Gabriela Da Silva Xavier
University of Birmingham

Obesity (Silver Spring). 2023 Aug 03.

Circadian misalignment increases 24-hour acylated ghrelin in chronic shift workers: a randomized crossover trial.

Jingyi Qian, Christopher J Morris, Rosanna Caputo, Frank A J L Scheer.

OBJECTIVE: Shift workers typically experience misalignment between their circadian system and behavioral/environmental cycles and have an increased risk for obesity. Experimental studies in non-shift workers have suggested that circadian misalignment can disrupt energy balance regulation. This study examined the impact of circadian misalignment in the most relevant population, i.e., chronic shift workers.METHODS: Seven healthy chronic night shift workers underwent a randomized crossover study with two 3-day laboratory protocols: a night work protocol including 12-hour inverted behavioral/environmental cycles (circadian misalignment) and a day work protocol (circadian alignment).
RESULTS: Circadian misalignment led to a ~17% increase in 24-hour acylated ghrelin levels in the chronic shift workers (p = 0.009). Consistently, circadian misalignment resulted in ~14% higher hunger at breakfast in the night shift (p = 0.04). Circadian misalignment did not significantly change fasting and postprandial energy expenditure or respiratory exchange ratio (all p > 0.32). Unexpectedly, 24-hour behavioral activity levels were ~38% higher (p < 0.0001) during circadian misalignment, despite a concurrent increase in sleepiness (p = 0.03).
CONCLUSIONS: These results reveal that circadian misalignment, while carefully controlling for dietary intake, increases acylated ghrelin in chronic shift workers. Further studies should test whether the observed acute effects of circadian misalignment in chronic shift workers contribute to their increased obesity risk in the long term.

DOI: https://doi.org/10.1002/oby.23838

Neuroendocrinology. 2023 Jul 29.

Circadian clock genes are regulated by rhythmic corticosterone at physiological levels in the rat hippocampus.

Tenna Bering, Aurea Susana Blancas-Velazquez, Martin Fredensborg Rath.

INTRODUCTION: In the hippocampus, clock gene expression is important for memory and mood; however, the signaling mechanism controlling clock gene expression in the hippocampus is unknown. Recent findings suggest that circadian glucocorticoid rhythms driven by the suprachiasmatic nucleus (SCN) control rhythmic clock gene expression in neurons; in addition, dexamethasone modulates hippocampal clock gene expression. We therefore hypothesized that oscillations of clock genes in the hippocampus could be driven by SCN-controlled circadian rhythms in glucocorticoids.METHODS: Temporal profiles of hippocampal clock gene expression were established by qRT-PCR on rat hippocampi, while cellular distribution was established by in situ hybridization. To determine the effect of rhythmic glucocorticoids on hippocampal clock gene expression, the SCN was lesioned, adrenal glands removed and a 24h exogenous corticosterone rhythm at physiological levels was reestablished by use of a programmable infusion pump.
RESULTS: Daily rhythms were detected for Per1, Per2, Bmal1, Nr1d1, and Dbp, while clock gene products were confirmed in both the hippocampus proper and the dentate gyrus. In sham controls, differential hippocampal expression of Per1 and Dbp between ZT3 and ZT15 was detectable. This rhythm was abolished by SCN-lesion; however, reestablishing the natural rhythm in corticosterone restored differential rhythmic expression of both Per1 and Dbp. Further, a 6h phase-delay in the corticosterone profile caused a predictable shift in expression of Nr1d1.
CONCLUSION: Our data show that rhythmic corticosterone can drive hippocampal clock gene rhythms suggesting that the SCN regulates the circadian oscillator of the hippocampus by controlling the circadian rhythm in circulating glucocorticoids.

DOI: https://doi.org/10.1159/000533151