It has been found from UC Irvine researchers that our own body clock helps regulate energy levels in cells. The findings have far-reaching implications that can be helpful in treating many diseases and conditions.
Paolo Sassone-Corsi, Distinguished Professor and Chair of Pharmacology and his research team has found that the proteins involved with circadian rhythms and metabolism are intrinsically linked and dependent upon each other.
“Our circadian rhythms and metabolism are closely partnered to ensure that cells function properly and remain healthy,” Sassone-Corsi said. “This discovery opens a new window for us to understand how these two fundamental processes work together, and it can have a great impact on new treatments for diseases caused by cell energy deficiencies.”
Circadian rhythms govern fundamental physiological functions. The circadian clocks are the essential time-tracking systems in our bodies that anticipate environmental changes and adapt to the appropriate time of day. Disruption of these rhythms can profoundly influence human health.
Sassone-Corsi already had identified that the enzyme protein CLOCK is an essential molecular gear of the circadian machinery and interacts with a protein, SIRT1, which senses cell energy levels and modulates aging and metabolism.
In the recent study it was found that CLOCK works in balance with SIRT1 to direct activity in a cell pathway by which metabolic proteins send signals called the NAD+ salvage pathway. In turn, a key protein in that pathway, NAMPT, helps control CLOCK levels, creating a tightly regulated codependency between our circadian clock and metabolism.
“When the balance between these two vital processes is upset, normal cellular function can be disrupted,” Sassone-Corsi said. “And this can lead to illness and disease.”
The findings suggest that proper sleep and diet may help maintain or rebuild this balance, he said, and also help explain why lack of rest or disruption of normal sleep patterns can increase hunger, leading to obesity-related illnesses and accelerated aging.
Adapted from materials provided by University of California – Irvine.