For the first time, researchers at the Georgia Health Sciences University in Augusta have found that that obesity might shut down a key gene clock that regulates the cardiovascular system.
Humans and animals are essentially programmed to physiologically respond to a day/night cycles based on the 24-hour rotation of the planet.
AdvertisementIndeed, there is a molecular basis that precisely controls rhythms, a group of genes dubbed the circadian clock, including one molecule also aptly named 'Clock'.
In obese individuals, the natural circadian rhythms are believed to be disrupted.
With obesity known to affect at least the eat/sleep cycles, Shuiqing Qiu and other researchers determined whether obesity might also affect the molecular components of the clock that governs the vascular system.
They conducted their research in two phases.
In phase I, they examined the circadian variation in the cardiovascular chamber of three groups of mice (lean, obese and diabetic) at three time intervals: early morning, mid-day and evening, and measured the gene expression in the cardiovascular genes during these times.
In the lean animals they found evidence of a cardiovascular rhythm.
By contrast, they found this rhythm was lost in obese animals.
In phase II, the team used the data to examine whether the lack of rhythmic response could translate into a cardiovascular defect. They did so by examining a series of specific molecules from the cardiovascular clock genes and by measuring the acceleration of the genes in the blood vessels.
In the lean animals they found that a key regulator of circadian rhythm, a gene called Clock, was high at 7:00 a.m. and low at 7:00 p.m.
In the obese animals the expression of the gene remained flat throughout the 24-hour cycle.
"Based on the results of this study we now know that obesity impairs the clock machinery of the vasculature system and that correlates with a variation in expression of cardiovascular genes and their loss of the circadian rhythm," said David Stepp, a senior researcher on the team.
The findings were presented at the Experimental Biology 2011 meeting at Washington, DC.
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