RYGB (roux-en-y gastric bypass) has been reported to reverse type 2 diabetes (T2DM) immediately after surgery before any significant weight loss. In addition, a growing number of patients have been recognized with life-threatening hyperinsulinemic hypoglycemia several years following their surgery. While the mechanisms by which RYGB improves glucose metabolism or alters islet cell function in patients after RYGB are not understood, recent studies suggest that increased secretion of GI hormones, primarily glucagon-like peptide 1 (GLP-1), as well as alteration in neural activity may contribute to enhanced insulin secretion in general, and to a greater extent in patients with hypoglycemia. The proposed research is designed to address the role of RYGB on insulin secretion by evaluating the contribution of stimulatory factors (neural and GI hormone) on islet cell function and the islet cell responsiveness to the physiologic stimulatory factors, in RYGB patients with and without hypoglycemia and non-operated controls.
Hypoglycemic RYGB patients with documented blood glucose level <50 mg/dl
Asymptomatic individuals with bariatric surgery
Healthy non-surgical patients with no personal history of diabetes
Subjects must physically be able to come to our clinical research center at Cedars-Sinai Medical Center
Active heart, lung, liver, gastrointestinal or kidney disease; unable to give informed consent; pregnancy; uncontrolled high blood pressure or high cholesterol; significant anemia (hemoglobin <11g/dL); prisoners or institutionalized individuals; type 2 diabetes melitis; development of any serious medical or psychiatric illness during recruitment or studies;
RYGB patients will also be disqualified if they have gastric outlet obstruction or severe diarrhea
Healthy non-surgical patients with personal history of diabetes
History of glaucoma
Crossover
Exendin-(9-39)
DrugA physiological study to evaluate the role of GLP-1 signaling in glucose tolerance and insulin secretion
Atropine
DrugA physiological study to evaluate the effect of neural activation on insulin secretion and glucose metabolism
GLP-1 and GIP
DrugA physiological study to evaluate the beta-cell sensitivity to different doses of exogenous gut hormones
Gut hormones and neural signaling contribution to insulin secretion rate and glucose tolerance
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