What a precise machine the body is. Although it is amazingly flexible, the human body also has specific regimens and timetables that when fiddled with, can throw everything off.
In most organisms, biological timekeeping is the task of the master clock. Known as the "circadian oscillator," the clock quietly ticks away and coordinates the biological processes to the rhythm of a 24-hour day. Along with this biological Big Ben, we humans have other clocks that work in tandem to keep our bodies doing what they are supposed to be doing; one of those extras is a food clock.
Known technically as the "food-entrainable oscillator," the food clock is a collection of interacting genes and molecules that help us best utilize our nutritional intake. It is the master of the genes that help in all things sustenance — like the absorption and dispersal of nutrients. It is there to anticipate and help map out our eating patterns. We feel hungry around lunchtime because the ol’ food-entrainable oscillator is beginning to turn on the right genes and turn off others in preparation for an influx of nutrients.
The food clock is basically calibrated to prime hunting and foraging hours — that is, daylight — but it can be reset over time if someone changes his eating patterns. Graveyard shifts, jet lag and midnight snacking can upset the food clock. Holiday binge eating can disturb it too.
Now a new study by researchers at UCSF is helping to reveal how this clock works on a molecular level. Published this month in the journal Proceedings of the National Academy of Sciences, the UCSF team reveals that a protein called PKCγ is crucial in resetting the food clock when our eating patterns change.
The researchers analyzed normal laboratory mice given food only during their regular sleeping hours; the mice adjusted their food clocks over time and began to wake up from sleeping in anticipation of their new mealtime. But mice lacking the PKCγ gene did not respond to changes in their mealtime; instead, they slept right through it.
The team discovered that there was a molecular basis for this phenomenon: the PKCγ protein binds to another molecule called BMAL and stabilizes it, which shifts the clock in time.
The work has implications for understanding the molecular basis of diabetes, obesity and other metabolic syndromes because a desynchronized food clock may serve as part of the pathology underlying these disorders, said Dr. Louis Ptacek, the John C. Coleman Distinguished Professor of Neurology at UCSF and a Howard Hughes Medical Institute investigator.
"Understanding the molecular mechanism of how eating at the 'wrong' time of the day desynchronizes the clocks in our body can facilitate the development of better treatments for disorders associated with night-eating syndrome, shift work and jet lag," he added.
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