Serotonin Regulates De Novo Lipogenesis in Adipose Tissues through Serotonin Receptor 2A.


Journal

Endocrinology and metabolism (Seoul, Korea)
ISSN: 2093-5978
Titre abrégé: Endocrinol Metab (Seoul)
Pays: Korea (South)
ID NLM: 101554139

Informations de publication

Date de publication:
06 2020
Historique:
received: 27 11 2019
accepted: 07 04 2020
entrez: 4 7 2020
pubmed: 4 7 2020
medline: 12 6 2021
Statut: ppublish

Résumé

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. 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. 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. These data suggest that the inhibition of serotonin signaling might be an effective strategy in obesity.

Sections du résumé

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.

Identifiants

pubmed: 32615731
pii: EnM.2020.35.2.470
doi: 10.3803/EnM.2020.35.2.470
pmc: PMC7386107
doi:

Substances chimiques

Htr2a protein, mouse 0
Receptor, Serotonin, 5-HT2A 0
Serotonin Receptor Agonists 0
Serotonin 333DO1RDJY
Tph1 protein, mouse EC 1.14.16.4
Tryptophan Hydroxylase EC 1.14.16.4

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

470-479

Commentaires et corrections

Type : ErratumIn

Références

J Diabetes Investig. 2016 Jan;7(1):32-41
pubmed: 26816599
Nature. 2006 Dec 14;444(7121):875-80
pubmed: 17167476
Nat Commun. 2018 Nov 16;9(1):4824
pubmed: 30446669
Mol Endocrinol. 2010 Oct;24(10):1978-87
pubmed: 20719859
Cell. 2008 Nov 28;135(5):825-37
pubmed: 19041748
Cold Spring Harb Protoc. 2010 Jun;2010(6):pdb.prot5439
pubmed: 20516177
FASEB J. 2013 Jan;27(1):277-87
pubmed: 23047894
Science. 2003 Jan 3;299(5603):76
pubmed: 12511643
Gastroenterology. 2007 Jan;132(1):397-414
pubmed: 17241888
JAMA. 2013 Jan 2;309(1):71-82
pubmed: 23280227
Cell Rep. 2014 Dec 11;9(5):1584-1593
pubmed: 25466254
Int J Obes (Lond). 2014 May;38(5):724-9
pubmed: 23900445
Diabetes. 2013 Mar;62(3):864-74
pubmed: 23321074
Nat Med. 2015 Feb;21(2):166-72
pubmed: 25485911
Int J Obes (Lond). 2018 Nov;42(11):1880-1889
pubmed: 29568107
Obesity (Silver Spring). 2012 Jan;20(1):233-8
pubmed: 21836641
Cell Metab. 2012 Nov 7;16(5):588-600
pubmed: 23085101
Endocrinology. 2010 Jun;151(6):2408-10
pubmed: 20489051
Nat Commun. 2015 Apr 13;6:6794
pubmed: 25864946
Cell Metab. 2011 Mar 2;13(3):249-59
pubmed: 21356515

Auteurs

Ko Eun Shong (KE)

Biomedical Science and Engineering Interdisciplinary Program, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Korea.

Chang-Myung Oh (CM)

Department of Biomedical Science and Engineering, Gwangju Institute of Science and Technology, Gwangju, Korea.

Jun Namkung (J)

Department of Biochemistry, Yonsei University Wonju College of Medicine, Wonju, Korea.

Sangkyu Park (S)

Department of Precision Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea.

Hail Kim (H)

Biomedical Science and Engineering Interdisciplinary Program, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Korea.
Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Korea.

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Classifications MeSH