Augmented capacity for peripheral serotonin release in human obesity.
Richard L Young1,2, Amanda L Lumsden3, Alyce M Martin3
1Adelaide Medical School, The University of Adelaide, Adelaide, SA, 5005, Australia.
International Journal of Obesity (2005)
|March 24, 2018
Summary
Obese individuals have increased serotonin (5-HT) production in the small intestine, contributing to obesity and dysglycemia. This gut-derived 5-HT plays a significant role in the development of these conditions.
Area of Science:
- Gastroenterology
- Metabolic Health
- Endocrinology
Background:
- Animal studies suggest gut serotonin (5-HT) influences metabolism and obesity.
- Human evidence linking elevated plasma 5-HT to obesity is limited.
Purpose of the Study:
- To investigate plasma 5-HT levels and enterochromaffin (EC) cell function in obese versus non-obese individuals.
- To explore the relationship between gut-derived 5-HT, body mass, and glycemic control.
Main Methods:
- Measured plasma 5-HT concentrations during intraduodenal glucose infusion in obese and control subjects.
- Assessed duodenal EC cell activation (pERK), TPH1 expression, and 5-HT content in gut tissue samples.
Main Results:
- Obese subjects exhibited twofold higher plasma 5-HT levels and increased duodenal EC cell density and activation.
- Elevated 5-HT correlated positively with BMI and HbA1c.
- TPH1 expression in the duodenum was higher in obese individuals.
Conclusions:
- Human obesity is associated with enhanced proximal small intestinal 5-HT production and release.
- Gut-derived 5-HT is implicated as a key factor in the pathogenesis of obesity and dysglycemia.
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