Student Article High School Science Journal Author: Pavitra Viswanathan

NFAT: A New, Feasible, Aggressive Treatment?

August 05, 2007

Diabetes is one of the most serious global health concerns today. A growing problem in both developed and third world countries, diabetes mellitus results when the body develops a deficiency in insulin levels. Insulin, a pancreatic hormone, is responsible for facilitating the metabolism of food by encouraging cells throughout the body to reap glucose from the bloodstream. Insulin’s instrumental role in providing glucose to the various organ tissues allows cellular respiration to occur and produce the energy necessary to conduct essential processes.

      However, in diabetic individuals, the insulin hormone is reduced in number or weakened in responsiveness, and therefore fails to efficiently stimulate the uptake of glucose. A decrease in insulin activity reduces glucose absorption, increases glycogen breakdown in the liver, and raises the individual’s overall blood sugar level. When excess amounts of glucose in the blood upset homeostasis in the body, a number of harmful consequences follow, including potential damage to the kidneys.

      As the number of diabetic individuals in the U.S. shockingly surpasses 20 million, the intensity in the race to identify the cause of and cure for this disorder increases. Recently, Stanford University announced a major breakthrough in diabetic research. The team declared that a protein called calcineurin is responsible for activating pancreatic beta cells, which produce insulin hormones. A series of experiments on mice found that mice lacking calcineurin developed diabetic conditions shortly after birth. The absence of calcineurin prevented the production of more pancreatic beta cells (necessary as the body mass of each growing mouse increased) and limited the amount of insulin produced by each beta cell. However, mice avoided these symptoms when exposed to calcineurin’s partner protein, NFAT, which allowed beta cells to continue multiplying and producing insulin as though calcineurin was present. Scientists concluded that by activating NFAT, individuals could compensate for a lack of calcineurin, and defend themselves against the damaging effects of diabetes by preventing an increase in blood sugar level. Currently, research is underway to evaluate the feasibility and effectiveness of supplementing diabetic individuals with regular doses of NFAT to stimulate the production of insulin. Additionally, researchers are exploring ways to manipulate NFAT to perform the opposite function: suppressing hyperactive insulin production in individuals diagnosed with hypoglycaemia. Have we finally arrived at a cure for this widespread health condition? Further research in this field is alone capable of answering this evasive question.

 
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