My inventive idea is to use a therapeutic molecule that slows gastric emptying for the treatment of functional dyspepsia in non-diabetic patients. This contrarian idea is based on our research of gastric emptying which shows that 30% of non-diabetic patients referred for gastric emptying studies due to gastrointestinal symptoms have elevated postprandial glycemic excursions and that elevated postprandial glycemic excursions are due to rapid gastric emptying of the carbohydrate portion of the meal. Based on our observations and recording of symptoms, an unexpectedly high number of patients referred for gastric emptying studies have previously undocumented elevated glycemic excursions consistent with rapid gastric emptying, and this rapid gastric emptying is frequently associated with significant pain during the first hour of our study.
It is my hypothesis that a therapeutic agent that slows down this rapid gastric emptying offers the excellent potential to alleviate these postprandial symptoms. These agents will also lower the abnormally elevated postprandial rise in glucose and blunt any feedback from elevated glucose levels and therefore smooth out these patients overall gastric emptying rate of both carbohydrates, proteins and fats. Since these patients that have functional dyspepsia, rapid gastric emptying and elevated postprandial glucose levels are at increase risk of future development of diabetes, this treatment which will delay gastric emptying and lower postprandial glucose levels likely have a preventative effect in these patients on their future development of diabetes.