Endoscopy, Obesity, Morbid
Conditions
Brief summary
In the stomach, the ghrelin-containing cells are more abundant in the fundus than in the pylorus originally termed X/A-like cells. These X/A-like cells account for approximately 20 % of the endocrine cell population in adult oxyntic glands. Ghrelin enhances the secretion of growth hormone, the stimulation of appetite and food intake, the modulation of gastric acid secretion & motility and the endocrine and exocrine pancreatic secretions.
Detailed description
Ghrelin is 28 amino acid peptide hormone, approximately 70 % of circulating ghrelin is secreted by the stomach, with most of the remainder originating in duodenum, jejunum, and ileum. Lower amount of secretion outside the gut, including hypothalamus (arcuate nucleus and paraventricular nucleus), pituitary, lung, adrenal cortex, kidney, bone, testis, placenta and pancreatic islet cells Ghrelin enhances the secretion of growth hormone, the stimulation of appetite and food intake, the modulation of gastric acid secretion & motility and the endocrine and exocrine pancreatic secretions. Synthetic ghrelin imitative was shown to increase fat deposition and appetite through an action at the level of the hypothalamus arcuate nucleus mainly the orexigenic neuropeptide Y (NPY) neurons. Alterations of ghrelin play an important role in appetite fluctuation following meals. The secretion of ghrelin by the stomach depends largely on the nutritional state. Ghrelin levels show pre-prandial increases and postprandial decreases. Low systemic ghrelin levels have been reported in untreated hyperthyroidism, in male hypogonadism, in the polycystic ovary syndrome, or after total gastrectomy \[5, 6\].
Interventions
reduction of ghrelin rich gastric mucosa with band ligation or argon plasma
Sponsors
Study design
Intervention model description
endoscopic reduction of ghrelin rich gastric mucosa either with 1. band ligation (group 1; n=16) and diet control 2. argon plasma mediated reduction and diet control (group 2; n=16) 3. control group exposed to low caloric diet and exercise (group 3; n=16).
Eligibility
Inclusion criteria
* body mass index more than 25 * diagnosis of diabetes mellitus. * diagnosis of cardio-metabolic syndrome. * fatty liver disease diagnosed by abdominal ultrasound.
Exclusion criteria
* use of drugs which induce insulin resistance, diabetes and hepatic steatosis. * excess alcohol consumption. * chronic gastritis, active peptic ulcer. * malignancy. * depression and severe psychological disorders * inability to give informed consent. * coagulopathy (INR more than 1.5, platelets less than 50000 per cmm). * severe cardiopulmonary comorbidity.
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| Number of patients with significant weight reduction | 6 month | significant weight reduction of more than 10% of baseline body weight measured in kilograms |
Other
| Measure | Time frame | Description |
|---|---|---|
| Number of patients with improved insulin resistance | 6 months | significant decrease in insulin resistance through assessing Homeostatic Model Assessment for Insulin Resistance, calculated by using the following formula: fasting glucose (mg/dL) X fasting insulin (µU/mL) / 405 |
Countries
Egypt