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Diabetes tied to altering of the heart's circadian clock

New Orleans, LA -- A new research study has found that diabetes, the cause of numerous heart disorders, likely disrupts the organ's circadian clock. This could lead to the heart failing to initiate important stimuli to several internal and external environmental changes, thereby contributing to heart failure.

Some 143 million patients worldwide are diagnosed with diabetes, almost five times more than estimates of ten years ago. Heart disease, often presenting as disease of the heart muscle (cardiomyopathy) is the leading cause of death among patients with diabetes mellitus. Diabetes, in turn, is the disease most associated with heart failure, and adversely affects outcomes of cardiovascular disease.

Background

Nearly 300 years ago, researchers found that almost all cells possess some kind of intrinsic and self-sustained "clocks" allowing perception of the time of day, independent of external influences. These internal clocks provide the selective advantage of anticipation, allowing an organism to prepare for an expected "stimulus" (such as activity, feeding, or light intensity for a photosynthetic organism) at a given time of the day. In order to maintain their advantageous nature, clocks are reset by environmental cues known as "zeitgebers," that enable the organism to become synchronized with its surroundings.

Mammals possess both a central clock numerous peripheral clocks. The former is located in the suprachiasmatic nucleus (SCN) where a central pacemaker perceives light signals via the retina, which resets its mechanism. Peripheral clocks are those clocks located within other regions of the organism besides the SCN. The central and peripheral clocks require synchronization; zeitgebers involved in the process are light for the central clock, and neurohumoral factors for the peripheral clocks. Several candidates have been suggested as the zeitgebers for peripheral clocks, including glucocorticoids, retinoic acid and melaton
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Contact: Donna Krupa
703-967-2751
American Physiological Society
22-Apr-2002


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