Author information
1 Division of Endocrinology and Metabolism, Department of Medicine, McMaster University, Hamilton, Ontario, Canada.
2 Centre for Metabolism, Obesity and Diabetes Research, McMaster University, Hamilton, Ontario, Canada.
3 Department of Biology, Northeastern University, Boston, MA, United States of America.
4 College of Medicine and Public Health, Flinders University, Bedford Park, SA, Australia.
5 Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, Ontario, Canada.
6 Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada.
7 Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, Ontario, Canada.
Abstract
Serotonin is a phylogenetically ancient biogenic amine that has played an integral role in maintaining energy homeostasis for billions of years. In mammals, serotonin produced within the central nervous system regulates behavior, suppresses appetite and promotes energy expenditure by increasing sympathetic drive to brown adipose tissue. In addition to these central circuits, emerging evidence also suggests an important role for peripheral serotonin as a factor that enhances nutrient absorption and storage. Specifically, glucose and fatty acids stimulate the release of serotonin from the duodenum promoting gut peristalsis and nutrient absorption. Serotonin also enters the blood stream and interacts with multiple organs, priming the body for energy storage by promoting insulin secretion, de novo lipogenesis in the liver and white adipose tissue, while reducing lipolysis and the metabolic activity of brown and beige adipose tissue. Collectively, peripheral serotonin acts as an endocrine factor to promote the efficient storage of energy by upregulating lipid anabolism. Pharmacological inhibition of serotonin synthesis or signaling in key metabolic tissues are potential drug targets for obesity and non-alcoholic fatty liver disease.