Serotonin signals through a gut-liver axis to regulate hepatic steatosis
Nonalcoholic fatty liver disease (NAFLD) is increasing in worldwide prevalence, closely tracking the obesity epidemic, but specific pharmaceutical treatments for NAFLD are lacking. Defining the key molecular pathways underlying the pathogenesis of NAFLD is essential for developing new drugs. Here we...
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| Vydáno v: | Nature communications Ročník 9; číslo 1; s. 4824 - 9 |
|---|---|
| Hlavní autoři: | , , , , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
London
Nature Publishing Group UK
16.11.2018
Nature Publishing Group Nature Portfolio |
| Témata: | |
| ISSN: | 2041-1723, 2041-1723 |
| On-line přístup: | Získat plný text |
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| Abstract | Nonalcoholic fatty liver disease (NAFLD) is increasing in worldwide prevalence, closely tracking the obesity epidemic, but specific pharmaceutical treatments for NAFLD are lacking. Defining the key molecular pathways underlying the pathogenesis of NAFLD is essential for developing new drugs. Here we demonstrate that inhibition of gut-derived serotonin synthesis ameliorates hepatic steatosis through a reduction in liver serotonin receptor 2A (HTR2A) signaling. Local serotonin concentrations in the portal blood, which can directly travel to and affect the liver, are selectively increased by high-fat diet (HFD) feeding in mice. Both gut-specific
Tph1
knockout mice and liver-specific
Htr2a
knockout mice are resistant to HFD-induced hepatic steatosis, without affecting systemic energy homeostasis. Moreover, selective HTR2A antagonist treatment prevents HFD-induced hepatic steatosis. Thus, the gut TPH1-liver HTR2A axis shows promise as a drug target to ameliorate NAFLD with minimal systemic metabolic effects.
No effective pharmacological treatments exist for nonalcoholic fatty liver disease (NAFLD). Here, the authors show that serotonin concentration in the portal blood is increased in nine human subjects and in mice fed a high-fat diet, and that local serotonin signaling ablation, either genetically or with an antagonist, prevents hepatic steatosis in mice. |
|---|---|
| AbstractList | No effective pharmacological treatments exist for nonalcoholic fatty liver disease (NAFLD). Here, the authors show that serotonin concentration in the portal blood is increased in nine human subjects and in mice fed a high-fat diet, and that local serotonin signaling ablation, either genetically or with an antagonist, prevents hepatic steatosis in mice. Nonalcoholic fatty liver disease (NAFLD) is increasing in worldwide prevalence, closely tracking the obesity epidemic, but specific pharmaceutical treatments for NAFLD are lacking. Defining the key molecular pathways underlying the pathogenesis of NAFLD is essential for developing new drugs. Here we demonstrate that inhibition of gut-derived serotonin synthesis ameliorates hepatic steatosis through a reduction in liver serotonin receptor 2A (HTR2A) signaling. Local serotonin concentrations in the portal blood, which can directly travel to and affect the liver, are selectively increased by high-fat diet (HFD) feeding in mice. Both gut-specific Tph1 knockout mice and liver-specific Htr2a knockout mice are resistant to HFD-induced hepatic steatosis, without affecting systemic energy homeostasis. Moreover, selective HTR2A antagonist treatment prevents HFD-induced hepatic steatosis. Thus, the gut TPH1-liver HTR2A axis shows promise as a drug target to ameliorate NAFLD with minimal systemic metabolic effects. Nonalcoholic fatty liver disease (NAFLD) is increasing in worldwide prevalence, closely tracking the obesity epidemic, but specific pharmaceutical treatments for NAFLD are lacking. Defining the key molecular pathways underlying the pathogenesis of NAFLD is essential for developing new drugs. Here we demonstrate that inhibition of gut-derived serotonin synthesis ameliorates hepatic steatosis through a reduction in liver serotonin receptor 2A (HTR2A) signaling. Local serotonin concentrations in the portal blood, which can directly travel to and affect the liver, are selectively increased by high-fat diet (HFD) feeding in mice. Both gut-specific Tph1 knockout mice and liver-specific Htr2a knockout mice are resistant to HFD-induced hepatic steatosis, without affecting systemic energy homeostasis. Moreover, selective HTR2A antagonist treatment prevents HFD-induced hepatic steatosis. Thus, the gut TPH1-liver HTR2A axis shows promise as a drug target to ameliorate NAFLD with minimal systemic metabolic effects. Nonalcoholic fatty liver disease (NAFLD) is increasing in worldwide prevalence, closely tracking the obesity epidemic, but specific pharmaceutical treatments for NAFLD are lacking. Defining the key molecular pathways underlying the pathogenesis of NAFLD is essential for developing new drugs. Here we demonstrate that inhibition of gut-derived serotonin synthesis ameliorates hepatic steatosis through a reduction in liver serotonin receptor 2A (HTR2A) signaling. Local serotonin concentrations in the portal blood, which can directly travel to and affect the liver, are selectively increased by high-fat diet (HFD) feeding in mice. Both gut-specific Tph1 knockout mice and liver-specific Htr2a knockout mice are resistant to HFD-induced hepatic steatosis, without affecting systemic energy homeostasis. Moreover, selective HTR2A antagonist treatment prevents HFD-induced hepatic steatosis. Thus, the gut TPH1-liver HTR2A axis shows promise as a drug target to ameliorate NAFLD with minimal systemic metabolic effects. No effective pharmacological treatments exist for nonalcoholic fatty liver disease (NAFLD). Here, the authors show that serotonin concentration in the portal blood is increased in nine human subjects and in mice fed a high-fat diet, and that local serotonin signaling ablation, either genetically or with an antagonist, prevents hepatic steatosis in mice. Nonalcoholic fatty liver disease (NAFLD) is increasing in worldwide prevalence, closely tracking the obesity epidemic, but specific pharmaceutical treatments for NAFLD are lacking. Defining the key molecular pathways underlying the pathogenesis of NAFLD is essential for developing new drugs. Here we demonstrate that inhibition of gut-derived serotonin synthesis ameliorates hepatic steatosis through a reduction in liver serotonin receptor 2A (HTR2A) signaling. Local serotonin concentrations in the portal blood, which can directly travel to and affect the liver, are selectively increased by high-fat diet (HFD) feeding in mice. Both gut-specific Tph1 knockout mice and liver-specific Htr2a knockout mice are resistant to HFD-induced hepatic steatosis, without affecting systemic energy homeostasis. Moreover, selective HTR2A antagonist treatment prevents HFD-induced hepatic steatosis. Thus, the gut TPH1-liver HTR2A axis shows promise as a drug target to ameliorate NAFLD with minimal systemic metabolic effects. No effective pharmacological treatments exist for nonalcoholic fatty liver disease (NAFLD). Here, the authors show that serotonin concentration in the portal blood is increased in nine human subjects and in mice fed a high-fat diet, and that local serotonin signaling ablation, either genetically or with an antagonist, prevents hepatic steatosis in mice. Nonalcoholic fatty liver disease (NAFLD) is increasing in worldwide prevalence, closely tracking the obesity epidemic, but specific pharmaceutical treatments for NAFLD are lacking. Defining the key molecular pathways underlying the pathogenesis of NAFLD is essential for developing new drugs. Here we demonstrate that inhibition of gut-derived serotonin synthesis ameliorates hepatic steatosis through a reduction in liver serotonin receptor 2A (HTR2A) signaling. Local serotonin concentrations in the portal blood, which can directly travel to and affect the liver, are selectively increased by high-fat diet (HFD) feeding in mice. Both gut-specific Tph1 knockout mice and liver-specific Htr2a knockout mice are resistant to HFD-induced hepatic steatosis, without affecting systemic energy homeostasis. Moreover, selective HTR2A antagonist treatment prevents HFD-induced hepatic steatosis. Thus, the gut TPH1-liver HTR2A axis shows promise as a drug target to ameliorate NAFLD with minimal systemic metabolic effects.Nonalcoholic fatty liver disease (NAFLD) is increasing in worldwide prevalence, closely tracking the obesity epidemic, but specific pharmaceutical treatments for NAFLD are lacking. Defining the key molecular pathways underlying the pathogenesis of NAFLD is essential for developing new drugs. Here we demonstrate that inhibition of gut-derived serotonin synthesis ameliorates hepatic steatosis through a reduction in liver serotonin receptor 2A (HTR2A) signaling. Local serotonin concentrations in the portal blood, which can directly travel to and affect the liver, are selectively increased by high-fat diet (HFD) feeding in mice. Both gut-specific Tph1 knockout mice and liver-specific Htr2a knockout mice are resistant to HFD-induced hepatic steatosis, without affecting systemic energy homeostasis. Moreover, selective HTR2A antagonist treatment prevents HFD-induced hepatic steatosis. Thus, the gut TPH1-liver HTR2A axis shows promise as a drug target to ameliorate NAFLD with minimal systemic metabolic effects. |
| ArticleNumber | 4824 |
| Author | Ju, Young Seok Park, Seongyeol Hwang, Inseon Choi, Chan Kim, Hyeongseok Park, Jun Yong Namkung, Jun Yadav, Vijay K. Park, Hye Jung Suh, Jae Myoung Kim, Hail Choi, Wonsuk Jeong, Ji-Seon Lim, Ajin Karsenty, Gerard Han, Kwang-Hyub Bang, Geul Kim, Young Hwan Park, Sangkyu Lee, Hye Won |
| Author_xml | – sequence: 1 givenname: Wonsuk surname: Choi fullname: Choi, Wonsuk organization: Graduate School of Medical Science and Engineering, KAIST – sequence: 2 givenname: Jun surname: Namkung fullname: Namkung, Jun organization: Graduate School of Medical Science and Engineering, KAIST, Department of Biochemistry, Yonsei University Wonju College of Medicine – sequence: 3 givenname: Inseon surname: Hwang fullname: Hwang, Inseon organization: Biomedical Science and Engineering Interdisciplinary Program, KAIST – sequence: 4 givenname: Hyeongseok surname: Kim fullname: Kim, Hyeongseok organization: Graduate School of Medical Science and Engineering, KAIST – sequence: 5 givenname: Ajin surname: Lim fullname: Lim, Ajin organization: Graduate School of Medical Science and Engineering, KAIST – sequence: 6 givenname: Hye Jung surname: Park fullname: Park, Hye Jung organization: Department of Internal Medicine, Yonsei University College of Medicine, Yonsei Liver Center, Severance Hospital – sequence: 7 givenname: Hye Won surname: Lee fullname: Lee, Hye Won organization: Department of Internal Medicine, Yonsei University College of Medicine, Yonsei Liver Center, Severance Hospital – sequence: 8 givenname: Kwang-Hyub surname: Han fullname: Han, Kwang-Hyub organization: Department of Internal Medicine, Yonsei University College of Medicine, Yonsei Liver Center, Severance Hospital – sequence: 9 givenname: Seongyeol surname: Park fullname: Park, Seongyeol organization: Graduate School of Medical Science and Engineering, KAIST – sequence: 10 givenname: Ji-Seon surname: Jeong fullname: Jeong, Ji-Seon organization: Center for Bioanalysis, Division of Metrology for Quality of Life, Korea Research Institute of Standards and Science – sequence: 11 givenname: Geul surname: Bang fullname: Bang, Geul organization: Biomedical Omics Group, Korea Basic Science Institute – sequence: 12 givenname: Young Hwan surname: Kim fullname: Kim, Young Hwan organization: Biomedical Omics Group, Korea Basic Science Institute – sequence: 13 givenname: Vijay K. surname: Yadav fullname: Yadav, Vijay K. organization: Department of Genetics and Development, Columbia University Medical Center – sequence: 14 givenname: Gerard orcidid: 0000-0002-9253-7627 surname: Karsenty fullname: Karsenty, Gerard organization: Department of Genetics and Development, Columbia University Medical Center – sequence: 15 givenname: Young Seok orcidid: 0000-0002-5514-4189 surname: Ju fullname: Ju, Young Seok organization: Graduate School of Medical Science and Engineering, KAIST – sequence: 16 givenname: Chan surname: Choi fullname: Choi, Chan organization: Department of Pathology, Chonnam National University Medical School – sequence: 17 givenname: Jae Myoung surname: Suh fullname: Suh, Jae Myoung organization: Graduate School of Medical Science and Engineering, KAIST, Biomedical Science and Engineering Interdisciplinary Program, KAIST – sequence: 18 givenname: Jun Yong orcidid: 0000-0001-6324-2224 surname: Park fullname: Park, Jun Yong email: drpjy@yuhs.ac organization: Department of Internal Medicine, Yonsei University College of Medicine, Yonsei Liver Center, Severance Hospital – sequence: 19 givenname: Sangkyu surname: Park fullname: Park, Sangkyu email: 49park@cku.ac.kr organization: Graduate School of Medical Science and Engineering, KAIST, Department of Biochemistry, College of Medicine, Catholic Kwandong University – sequence: 20 givenname: Hail orcidid: 0000-0002-6652-1349 surname: Kim fullname: Kim, Hail email: hailkim@kaist.edu organization: Graduate School of Medical Science and Engineering, KAIST, Biomedical Science and Engineering Interdisciplinary Program, KAIST, KAIST Institute for the BioCentury, KAIST |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30446669$$D View this record in MEDLINE/PubMed |
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| Snippet | Nonalcoholic fatty liver disease (NAFLD) is increasing in worldwide prevalence, closely tracking the obesity epidemic, but specific pharmaceutical treatments... No effective pharmacological treatments exist for nonalcoholic fatty liver disease (NAFLD). Here, the authors show that serotonin concentration in the portal... |
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| Title | Serotonin signals through a gut-liver axis to regulate hepatic steatosis |
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