Role of Neural and Hormonal Regulation Factors on Insulin Secretion After Gastric Bypass Surgery

This study is currently recruiting participants. (see Contacts and Locations)
Verified February 2013 by University of Cincinnati
Sponsor:
Collaborators:
David D'Alessio
Information provided by (Responsible Party):
Marzieh Salehi, University of Cincinnati
ClinicalTrials.gov Identifier:
NCT00992901
First received: October 7, 2009
Last updated: February 25, 2013
Last verified: February 2013
  Purpose

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.


Condition Intervention Phase
Post Bariatric Surgery
Hypoglycemia
Drug: Exendin-(9-39)
Drug: Atropine
Drug: GLP-1 and GIP
Phase 0

Study Type: Interventional
Study Design: Allocation: Non-Randomized
Intervention Model: Crossover Assignment
Masking: Open Label
Official Title: Hormonal and Neural Control of Insulin Secretion Following Gastric Bypass Surgery

Resource links provided by NLM:


Further study details as provided by University of Cincinnati:

Primary Outcome Measures:
  • Gut hormones and neural signaling contribution to insulin secretion rate and glucose tolerance [ Time Frame: Each individual will be evaluated with series of metabolic studies over time ] [ Designated as safety issue: No ]

Estimated Enrollment: 160
Study Start Date: October 2009
Estimated Primary Completion Date: July 2014 (Final data collection date for primary outcome measure)
Arms Assigned Interventions
Experimental: Exendin-(9-39)
To evaluate the role of GLP-1 signaling in glucose tolerance and insulin secretion
Drug: Exendin-(9-39)
Experimental: atropine
To evaluate the effect of neural activation on insulin secretion and glucose metabolism
Drug: Atropine
Experimental: GLP-1 and GIP
to evaluate the beta-cell sensitivity to different doses of exogenous gut hormones
Drug: GLP-1 and GIP

  Eligibility

Ages Eligible for Study:   18 Years to 65 Years
Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   Yes
Criteria

Inclusion Criteria:

  • 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 Children's Hospital Medical Center in Cincinnati

Exclusion Criteria:

  • active heart, lung, liver, gastrointestinal or kidney disease; unable to give informed consent; pregnancy; uncontrolled high blood pressure or high cholesterol; significant anemia; prisoners or institutionalized individuals; type 2 diabetes melitis; development of any serious medical or psychiatric illness during recruitment or studies;
  • for atropine portion of study = same as listed above plus history of glaucoma, myasthenia gravis, brain pathology, enlarged prostate in men, taking of medications that might interact with atropine and cannot be stopped;
  • for RYGB patients will also be disqualified if they have gastric outlet obstruction or severe diarrhea
  Contacts and Locations
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the Contacts provided below. For general information, see Learn About Clinical Studies.

Please refer to this study by its ClinicalTrials.gov identifier: NCT00992901

Contacts
Contact: Leslie M Baum, RN, BSN 513-558-0201 leslie.baum@uc.edu
Contact: Marzieh Salehi, MD 513-558-4444 marzieh.salehi@uc.edu

Locations
United States, Ohio
University of Cincinnati Recruiting
Cincinnati, Ohio, United States, 45267
Contact: Leslie M Baum, RN, BSN    513-558-0201    leslie.baum@uc.edu   
Contact: Marzieh Salehi, MD    513-558-4444    marzieh.salehi@uc.edu   
Principal Investigator: Marzieh Salehi, MD         
Cincinnati Children's Hospital Medical Center GCRC Recruiting
Cincinnati, Ohio, United States, 45229
Contact: Leslie M Baum, RN, BSN    513-558-0201    leslie.baum@uc.edu   
Contact: Marzieh Salehi, MD    513-558-4444    marzieh.salehi@uc.edu   
Principal Investigator: Marzieh Salehi, MD         
Veteran Affairs Medical Center GCRC Recruiting
Cincinnati, Ohio, United States, 45267
Contact: Leslie M Baum, RN, BSN    513-558-0201    leslie.baum@uc.edu   
Contact: Marzieh Salehi, MD    513-558-4444    marzieh.salehi@uc.edu   
Principal Investigator: Marzieh Salehi, MD         
Sponsors and Collaborators
University of Cincinnati
David D'Alessio
Investigators
Principal Investigator: Marzieh Salehi, MD University of Cincinnati
  More Information

No publications provided

Responsible Party: Marzieh Salehi, Assistant Professor, University of Cincinnati
ClinicalTrials.gov Identifier: NCT00992901     History of Changes
Other Study ID Numbers: DK083554
Study First Received: October 7, 2009
Last Updated: February 25, 2013
Health Authority: United States: Food and Drug Administration

Keywords provided by University of Cincinnati:
gastric bypass surgery
glucose tolerance
Insulin response to meal ingestion
Gut hormone and neural response to meal ingestion

Additional relevant MeSH terms:
Hypoglycemia
Glucose Metabolism Disorders
Metabolic Diseases
Atropine
Insulin
Adjuvants, Anesthesia
Central Nervous System Agents
Therapeutic Uses
Pharmacologic Actions
Anti-Arrhythmia Agents
Cardiovascular Agents
Bronchodilator Agents
Autonomic Agents
Peripheral Nervous System Agents
Physiological Effects of Drugs
Anti-Asthmatic Agents
Respiratory System Agents
Mydriatics
Parasympatholytics
Muscarinic Antagonists
Cholinergic Antagonists
Cholinergic Agents
Neurotransmitter Agents
Molecular Mechanisms of Pharmacological Action
Hypoglycemic Agents

ClinicalTrials.gov processed this record on July 24, 2014