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2018 ; 60
(3
): R115-R130
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Circadian rhythms in mitochondrial respiration
#MMPMID29378772
de Goede P
; Wefers J
; Brombacher EC
; Schrauwen P
; Kalsbeek A
J Mol Endocrinol
2018[Apr]; 60
(3
): R115-R130
PMID29378772
show ga
Many physiological processes are regulated with a 24-h periodicity to anticipate
the environmental changes of daytime to nighttime and vice versa. These 24-h
regulations, commonly termed circadian rhythms, among others control the
sleep-wake cycle, locomotor activity and preparation for food availability during
the active phase (daytime for humans and nighttime for nocturnal animals).
Disturbing circadian rhythms at the organ or whole-body level by social jetlag or
shift work, increases the risk to develop chronic metabolic diseases such as type
2 diabetes mellitus. The molecular basis of this risk is a topic of increasing
interest. Mitochondria are essential organelles that produce the majority of
energy in eukaryotes by converting lipids and carbohydrates into ATP through
oxidative phosphorylation. To adapt to the ever-changing environment,
mitochondria are highly dynamic in form and function and a loss of this
flexibility is linked to metabolic diseases. Interestingly, recent studies have
indicated that changes in mitochondrial morphology (i.e., fusion and fission) as
well as generation of new mitochondria are dependent on a viable circadian clock.
In addition, fission and fusion processes display diurnal changes that are
aligned to the light/darkness cycle. Besides morphological changes, mitochondrial
respiration also displays diurnal changes. Disturbing the molecular clock in
animal models leads to abrogated mitochondrial rhythmicity and altered
respiration. Moreover, mitochondrial-dependent production of reactive oxygen
species, which plays a role in cellular signaling, has also been linked to the
circadian clock. In this review, we will summarize recent advances in the study
of circadian rhythms of mitochondria and how this is linked to the molecular
circadian clock.
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