Role of Neural and Hormonal Regulation Factors on Insulin Secretion After Gastric Bypass Surgery
Hormonal and Neural Control of Insulin Secretion Following Gastric Bypass Surgery
The University of Texas Health Science Center at San Antonio
160 participants
Oct 1, 2009
INTERVENTIONAL
Conditions
Summary
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.
Eligibility
Plain Language Summary
Simplified for easier understanding
This summary was AI-generated to explain the trial in plain language. It is not medical advice. Always discuss eligibility with your doctor before enrolling in a clinical trial.
Interested in this trial?
Get notified about updates and connect with the research team.
Interventions
A physiological study to evaluate the role of GLP-1 signaling in glucose tolerance and insulin secretion
A physiological study to evaluate the effect of neural activation on insulin secretion and glucose metabolism
A physiological study to evaluate the beta-cell sensitivity to different doses of exogenous gut hormones
Locations(2)
View Full Details on ClinicalTrials.gov
For the most up-to-date information, visit the official listing.
NCT00992901