This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The Diabetes Control and Complications Trial (DCCT) demonstrated that most patients with T1DM should receive intensive treatment to lower the risks of complications. In younger children with diabetes, strict diabetes control is achieved at the expense of unacceptably high incidence of hypoglycemia. T1DM is considered a bihormonal disease wherein there is insulin deficiency and glucagon dysregulation resulting in post-prandial hyperglycemia and pre-prandial hypoglycemia. In addition to glucagon we are now learning of other hormones that may contribute to the dyshormonogenesis of diabetes. One such hormone is amylin. Amylin is secreted by beta cells and is an exclusive glucagon suppressor. Amylin deficiency and glucagon dysregulation in T1DM may result in abnormal glucose excursions often seen in T1DM. Current treatment of T1DM employs the manipulation of insulin pharmacokinetics and diet to normalize glucose excursions with limited success despite the use of newer insulin analogs and insulin pumps. This proposal aims at using a novel two pronged approach using pramlintide, a synthetic form of amylin to combat post-prandial hyperglycemia and glucagon injection to prevent pre-prandial hypoglycemia. This study for the first time will investigate the pharmacotherapeutic role of amylin and glucagon in the prevention of hyper and hypoglycemia in pediatric T1DM.
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