NCT00992901

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

• Status: Recruiting
• Phase: EARLY_Phase 1
• Study type: Interventional
• Enrollment: 160 (estimated)
• Sponsor: The University of Texas Health Science Center at San Antonio · Academic / Other
• Sex: All
• Age: 18 Years – 65 Years
• Healthy volunteers: Accepted

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.

Detailed description

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

Conditions

• Post Bariatricsurgery
• Hypoglycemia

Interventions

Type	Name	Description
DRUG	Exendin-(9-39)	A physiological study to evaluate the role of GLP-1 signaling in glucose tolerance and insulin secretion
DRUG	Atropine	A physiological study to evaluate the effect of neural activation on insulin secretion and glucose metabolism
DRUG	GLP-1 and GIP	A physiological study to evaluate the beta-cell sensitivity to different doses of exogenous gut hormones

Timeline

• Start date: 2009-10-01
• Primary completion: 2026-08-01
• Completion: 2027-08-01
• First posted: 2009-10-09
• Last updated: 2025-09-09

Locations

2 sites across 1 country: United States