Role of Neural and Hormonal Regulation Factors on Insulin Secretion After Gastric Bypass Surgery
This study is currently recruiting participants.
Verified February 2013 by University of Cincinnati
Sponsor:
University of Cincinnati
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
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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
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 May 23, 2013