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Erratum: Correction of Figure. Serotonin Regulates De Novo Lipogenesis in Adipose Tissues through Serotonin Receptor 2A
Ko Eun Shong, Chang-Myung Oh, Jun Namkung, Sangkyu Park, Hail Kim
Endocrinol Metab. 2020;35(3):672.   Published online August 6, 2020
DOI: https://doi.org/10.3803/EnM.2020.307
Corrects: Endocrinol Metab 2020;35(2):470
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Original Article
Endocrine Research
Serotonin Regulates De Novo Lipogenesis in Adipose Tissues through Serotonin Receptor 2A
Ko Eun Shong, Chang-Myung Oh, Jun Namkung, Sangkyu Park, Hail Kim
Endocrinol Metab. 2020;35(2):470-479.   Published online June 24, 2020
DOI: https://doi.org/10.3803/EnM.2020.35.2.470
Correction in: Endocrinol Metab 2020;35(3):672
  • 15,423 View
  • 296 Download
  • 34 Web of Science
  • 33 Crossref
AbstractAbstract PDFSupplementary MaterialPubReader   ePub   
Background
Obesity is defined as excessive fat mass and is a major cause of many chronic diseases such as diabetes, cardiovascular disease, and cancer. Increasing energy expenditure and regulating adipose tissue metabolism are important targets for the treatment of obesity. Serotonin (5-hydroxytryptophan [5-HT]) is a monoamine metabolite of the essential amino acid tryptophan. Here, we demonstrated that 5-HT in mature adipocytes regulated energy expenditure and lipid metabolism.
Methods
Tryptophan hydroxylase 1 (TPH1) is the rate-limiting enzyme during 5-HT synthesis in non-neural peripheral tissues. We generated adipose tissue-specific Tph1 knockout (Tph1 FKO) mice and adipose tissue-specific serotonin receptor 2A KO (Htr2a FKO) mice and analyzed their phenotypes during high-fat diet (HFD) induced obesity.
Results
Tph1 FKO mice fed HFD exhibited reduced lipid accumulation, increased thermogenesis, and resistance to obesity. In addition, Htr2a FKO mice fed HFD showed reduced lipid accumulation in white adipose tissue and resistance to obesity.
Conclusion
These data suggest that the inhibition of serotonin signaling might be an effective strategy in obesity.

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