Stomach accommodation and symptoms in obesity and octreotide
The development of obesity is the result of an imbalance between food intake and energy expenditure. The mechanisms that control food intake or energy expenditure are not fully understood. Signals that arise from the GI tract contribute to meal termination and, hence, determine meal size. One of the modulations of upper GI secretion, sensation, and motility is the neurotransmitter, somatostatin. Octreotide, the cyclized analog octapeptide, binds preferentially to type 2 somatostatin receptors. Some studies have shown the effects of somatostatin or the synthetic analog, octreotide, on human GI motor functions in health and disease states. To further this research area, a group of researchers from the Mayo Clinic compared the effects of octreotide and a placebo on postprandial symptoms, satiation, and gastric volumes in obese patients.
In a randomized, parallel-group, double-blind, placebo-controlled study, 26 obese but otherwise healthy subjects received 100 micrograms of octreotide or placebo simultaneously 30 minutes before each study. Studies were performed on two separate days and included validated noninvasive techniques: 99mTc-single photon emission computed tomography imaging to measure fasting stomach volume and gastric volume changes after 90 mL of water, 240 mL of Ensure, and a standardized nutrient drink test to measure the maximum tolerated volume and postprandial symptoms.
Relative to placebo, octreotide increased gastric volume after 90 mL of water, but fasting and gastric volume change post-Ensure and maximum tolerated volume of Ensure were not different. Octreotide decreased sensations of fullness and bloating and tended to reduce aggregate symptoms after the fully satiating meal.
In obese individuals, somatostatin analog significantly reduced postprandial sensations after a satiating meal without altering maximum tolerated meal volume or post-nutrient gastric volume, suggesting an effect on upper gut sensation. The data also suggest that different mechanisms come into play in the presence of nonnutrient or nutrient loads to the stomach. The role of somatostatin as a permissive factor in the development of obesity by reducing postprandial sensations deserves further study.
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