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New research led by the University of Oxford in the UK suggests it may be possible to speed up recovery from jet lag by targeting a mechanism that prevents the body clock adjusting quickly to changes in patterns of light and dark.
Working on mice, they found a protein called SIK1 acts as a buffer or brake to limit the effect of light on the body clock. When they blocked the activity of the protein, the mice adjusted faster to changes in their light/dark cycle.
One of the team leaders, Dr. Stuart Peirson from Oxford's Nuffield Laboratory of Ophthalmology, says they found a mechanism that "actively prevents the body clock from re-adjusting," and explains it makes sense to have such a system because it keeps the body clock stable:
"The clock needs to be sure that it is getting a reliable signal, and if the signal occurs at the same time over several days it probably has biological relevance. But it is this same buffering mechanism that slows down our ability to adjust to a new time zone and causes jet lag."
The study, which was funded by the Wellcome Trust and F. Hoffmann La Roche, was published online in the journal Cell on August 29th.
Nearly all living things have an internal body clock that syncs their biology to a 24-hour cycle, ensuring functions like sleeping and eating are correctly tuned to daily patterns of light and dark.
When we travel to a different time zone, this "circadian clock" takes time to adjust to the shifted pattern of day and night. This can take up to 1 day for every shifted hour, resulting in several days of fatigue and confusion.
Scientists have discovered that in mammals, the circadian clock is regulated by the brain's suprachiasmatic nuclei (SCN), which ensures every cell of the body dances to the same biological rhythm.
The SCN in turn is regulated by a system linked to the eyes that senses light to determine time of day and to keep the circadian clock tuned to local time.
But until this latest study, it was not clear exactly how SCN uses light to tune the body clock and why it takes so long for it to adjust when the pattern of light/dark shifts, such as when we jet to a new time zone.
The researchers decided to investigate this by looking at patterns of gene expression that affect the SCN in mice.
They found about 100 genes were involved in responding to light and dark, causing a sequence of molecular patterns that retuned the mice's circadian clocks.
They found that one molecule in particular, a protein called salt inducible kinase 1 (SIK1), acts like a buffer or brake to limit the effects of light on the circadian clock. And when they blocked SIK1 in the mice, the animals adjusted more quickly to changes in their light/dark cycle.
The researchers point out these findings do not mean that a cure for jet lag is going to be easy to find.
Professor Russell Foster, director of the Sleep and Circadian Neuroscience Institute at Oxford, who co-led the team with Dr. Peirson, says:
"We're still several years away from a cure for jet-lag, but understanding the mechanisms that generate and regulate our circadian clock gives us targets to develop drugs to help bring our bodies in tune with the solar cycle."
"Such drugs could potentially have broader therapeutic value for people with mental health issues," he adds.
In 2012, researchers in Australia reported a device resembling a pair of sunglasses that resets the body clock. The team said the device, which emits a soft green light onto the eyes, can counter the effects of jet lag and keep shift workers more alert.Written by Catharine Paddock PhD
Copyright: Medical News Today
Not to be reproduced without the permission of Medical News Today.
The CRTC1-SIK1 Pathway Regulates Entrainment of the Circadian Clock; Aarti Jagannath, Rachel Butler, Sofia I.H. Godinho, Yvonne Couch, Laurence A. Brown, Sridhar R. Vasudevan, Kevin C. Flanagan, Daniel Anthony, Grant C. Churchill, Matthew J.A. Wood, and others; Cell, 154(5) pp. 1100 - 1111, online 29 August 2013; DOI: 10.1016/j.cell.2013.08.004; Abstract
Additional source: Oxford University press release 30 August 2013.
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