Using micro positron emission tomography (microPET), Dr. Abbott and his team visualized the accumulation in the mouse thyroid of an iodine radioisotope in real-time. They found that absorption of the radioisotope in the thyroid was greatly impaired in mice lacking the KCNE2 gene. They believe that, normally, the KCNQ1-KCNE2 potassium channel helps another protein (the sodium/iodide symporter) to transport iodide into the thyroid.

Without the KCNQ1-KCNE2 potassium channel, the efficiency of iodide absorption by the thyroid is greatly reduced. Because iodide is an essential component of TH, this means that KCNE2 deletion also impairs TH production.

Future studies will now center on determining how applicable the research team's findings in the mouse are to the human population.

"While we have identified KCNQ1 and KCNE2 in both mouse and human thyroid, much additional work is required before we can fully understand how inherited mutations in the genes coding these proteins affect human thyroid function, how this in turn influences the health of human heart and other tissues, and how useful our discoveries will be in developing therapies to treat thyroid and thyroid-related human disease," explains Dr. Abbott.

Cardiac arrhythmias affect up to three million people in the United States. The majority of these suffer from atrial fibrillation, a chronic arrhythmia most often observed in the aging population. Ventricular arrhythmias account for the large majority of the 300,000 cases of sudden cardiac death annually in the United States. Thyroid dysfunction is estimated to affect one to four percent of the world's population.

Source: New York- Presbyterian Hospital/Weill Cornell Medical Center/Weill Cornell Medical College