Role of Neural and Hormonal Regulation Factors on Insulin Secretion After Gastric Bypass Surgery
| Status: | Recruiting |
|---|---|
| Conditions: | Other Indications, Endocrine, Gastrointestinal, Diabetes |
| Therapuetic Areas: | Endocrinology, Gastroenterology, Other |
| Healthy: | No |
| Age Range: | 18 - 65 |
| Updated: | 5/20/2018 |
| Start Date: | October 2009 |
| End Date: | July 2020 |
| Contact: | Marzieh Salehi, MD MS |
| Email: | salehi@uthscsa.edu |
| Phone: | 210-567-6691 |
Hormonal and Neural Control of Insulin Secretion Following Gastric Bypass Surgery
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.
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.
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
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
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
Cedars-Sinai Medical Center
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 (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
For administration of atropine, the following exclusions also apply:
- History of glaucoma
- Uncontrolled hypertension (any subjects with BP>140/90 and history of dyslipidemia
- Taking any medication that might interact with atropine and cannot be stopped will be
excluded from the study)
- Myasthenia gravis
- Brain pathology
- Enlarged prostate in men
We found this trial at
1
site
San Antonio, Texas 78229
Principal Investigator: Marzieh Salehi, MD, MS
Phone: 210-567-6691
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