No Cover Image

Journal article 94 views 28 downloads

Low resting metabolic rate and increased hunger due to β-MSH and β-endorphin deletion in a canine model

Marie T. Dittmann Orcid Logo, Gabriella Lakatos, Jodie F. Wainwright Orcid Logo, Jacek Mokrosinski, Eloise Cross Orcid Logo, I. Sadaf Farooqi, Natalie J. Wallis Orcid Logo, Lewis G. Halsey Orcid Logo, Rory Wilson Orcid Logo, Stephen O’Rahilly Orcid Logo, Giles S.H. Yeo Orcid Logo, Eleanor Raffan Orcid Logo

Science Advances, Volume: 10, Issue: 10

Swansea University Author: Rory Wilson Orcid Logo

  • 65193.VOR.pdf

    PDF | Version of Record

    Distributed under the terms of a Creative Commons Attribution CC-BY licence.

    Download (1.2MB)

Check full text

DOI (Published version): 10.1126/sciadv.adj3823

Abstract

Mutations that perturb leptin-melanocortin signaling are known to cause hyperphagia and obesity, but energy expenditure has not been well studied outside rodents. We report on a common canine mutation in pro-opiomelanocortin (POMC), which prevents production of β–melanocyte-stimulating hormone (β-MS...

Full description

Published in: Science Advances
ISSN: 2375-2548
Published: American Association for the Advancement of Science (AAAS) 2024
Online Access: Check full text

URI: https://cronfa.swan.ac.uk/Record/cronfa65193
Tags: Add Tag
No Tags, Be the first to tag this record!
first_indexed 2024-04-03T15:07:14Z
last_indexed 2024-04-03T15:07:14Z
id cronfa65193
recordtype SURis
fullrecord <?xml version="1.0" encoding="utf-8"?><rfc1807 xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:xsd="http://www.w3.org/2001/XMLSchema"><bib-version>v2</bib-version><id>65193</id><entry>2023-12-04</entry><title>Low resting metabolic rate and increased hunger due to β-MSH and β-endorphin deletion in a canine model</title><swanseaauthors><author><sid>017bc6dd155098860945dc6249c4e9bc</sid><ORCID>0000-0003-3177-0177</ORCID><firstname>Rory</firstname><surname>Wilson</surname><name>Rory Wilson</name><active>true</active><ethesisStudent>false</ethesisStudent></author></swanseaauthors><date>2023-12-04</date><deptcode>SBI</deptcode><abstract>Mutations that perturb leptin-melanocortin signaling are known to cause hyperphagia and obesity, but energy expenditure has not been well studied outside rodents. We report on a common canine mutation in pro-opiomelanocortin (POMC), which prevents production of β–melanocyte-stimulating hormone (β-MSH) and β-endorphin but not α-MSH; humans, similar to dogs, produce α-MSH and β-MSH from the POMC propeptide, but rodents produce only α-MSH. We show that energy expenditure is markedly lower in affected dogs, which also have increased motivational salience in response to a food cue, indicating increased wanting or hunger. There was no difference in satiety at a modified ad libitum meal or in their hedonic response to food, nor disruption of adrenocorticotropic hormone (ACTH) or thyroid axes. In vitro, we show that β-MSH signals comparably to α-MSH at melanocortin receptors. These data implicate β-MSH and β-endorphin as important in determining hunger and moderating energy expenditure and suggest that this role is independent of the presence of α-MSH.</abstract><type>Journal Article</type><journal>Science Advances</journal><volume>10</volume><journalNumber>10</journalNumber><paginationStart/><paginationEnd/><publisher>American Association for the Advancement of Science (AAAS)</publisher><placeOfPublication/><isbnPrint/><isbnElectronic/><issnPrint/><issnElectronic>2375-2548</issnElectronic><keywords/><publishedDay>8</publishedDay><publishedMonth>3</publishedMonth><publishedYear>2024</publishedYear><publishedDate>2024-03-08</publishedDate><doi>10.1126/sciadv.adj3823</doi><url>http://dx.doi.org/10.1126/sciadv.adj3823</url><notes/><college>COLLEGE NANME</college><department>Biosciences</department><CollegeCode>COLLEGE CODE</CollegeCode><DepartmentCode>SBI</DepartmentCode><institution>Swansea University</institution><apcterm>Another institution paid the OA fee</apcterm><funders>MR/S026193/1/MRC_/Medical Research Council/United Kingdom, MC_UU_12012/1/MRC_/Medical Research Council/United Kingdom, WT_/Wellcome Trust/United Kingdom, MC_UU_00014/1/MRC_/Medical Research Council/United Kingdom, MC_UU_12012/5/MRC_/Medical Research Council/United Kingdom.</funders><projectreference/><lastEdited>2024-04-03T16:08:57.2672471</lastEdited><Created>2023-12-04T10:18:27.5463291</Created><path><level id="1">Faculty of Science and Engineering</level><level id="2">School of Biosciences, Geography and Physics - Biosciences</level></path><authors><author><firstname>Marie T.</firstname><surname>Dittmann</surname><orcid>0000-0002-0470-5580</orcid><order>1</order></author><author><firstname>Gabriella</firstname><surname>Lakatos</surname><order>2</order></author><author><firstname>Jodie F.</firstname><surname>Wainwright</surname><orcid>0009-0004-1726-2442</orcid><order>3</order></author><author><firstname>Jacek</firstname><surname>Mokrosinski</surname><order>4</order></author><author><firstname>Eloise</firstname><surname>Cross</surname><orcid>0000-0002-9982-8056</orcid><order>5</order></author><author><firstname>I. Sadaf</firstname><surname>Farooqi</surname><order>6</order></author><author><firstname>Natalie J.</firstname><surname>Wallis</surname><orcid>0000-0001-9543-3711</orcid><order>7</order></author><author><firstname>Lewis G.</firstname><surname>Halsey</surname><orcid>0000-0002-0786-7585</orcid><order>8</order></author><author><firstname>Rory</firstname><surname>Wilson</surname><orcid>0000-0003-3177-0177</orcid><order>9</order></author><author><firstname>Stephen</firstname><surname>O’Rahilly</surname><orcid>0000-0003-2199-4449</orcid><order>10</order></author><author><firstname>Giles S.H.</firstname><surname>Yeo</surname><orcid>0000-0001-8823-3615</orcid><order>11</order></author><author><firstname>Eleanor</firstname><surname>Raffan</surname><orcid>0000-0002-1403-3538</orcid><order>12</order></author></authors><documents><document><filename>65193__29898__ac2336ceb4b14321928b4a3e44fddaab.pdf</filename><originalFilename>65193.VOR.pdf</originalFilename><uploaded>2024-04-03T15:57:59.7952096</uploaded><type>Output</type><contentLength>1259391</contentLength><contentType>application/pdf</contentType><version>Version of Record</version><cronfaStatus>true</cronfaStatus><documentNotes>Distributed under the terms of a Creative Commons Attribution CC-BY licence.</documentNotes><copyrightCorrect>true</copyrightCorrect><language>eng</language><licence>https://creativecommons.org/licenses/by/4.0/</licence></document></documents><OutputDurs/></rfc1807>
spelling v2 65193 2023-12-04 Low resting metabolic rate and increased hunger due to β-MSH and β-endorphin deletion in a canine model 017bc6dd155098860945dc6249c4e9bc 0000-0003-3177-0177 Rory Wilson Rory Wilson true false 2023-12-04 SBI Mutations that perturb leptin-melanocortin signaling are known to cause hyperphagia and obesity, but energy expenditure has not been well studied outside rodents. We report on a common canine mutation in pro-opiomelanocortin (POMC), which prevents production of β–melanocyte-stimulating hormone (β-MSH) and β-endorphin but not α-MSH; humans, similar to dogs, produce α-MSH and β-MSH from the POMC propeptide, but rodents produce only α-MSH. We show that energy expenditure is markedly lower in affected dogs, which also have increased motivational salience in response to a food cue, indicating increased wanting or hunger. There was no difference in satiety at a modified ad libitum meal or in their hedonic response to food, nor disruption of adrenocorticotropic hormone (ACTH) or thyroid axes. In vitro, we show that β-MSH signals comparably to α-MSH at melanocortin receptors. These data implicate β-MSH and β-endorphin as important in determining hunger and moderating energy expenditure and suggest that this role is independent of the presence of α-MSH. Journal Article Science Advances 10 10 American Association for the Advancement of Science (AAAS) 2375-2548 8 3 2024 2024-03-08 10.1126/sciadv.adj3823 http://dx.doi.org/10.1126/sciadv.adj3823 COLLEGE NANME Biosciences COLLEGE CODE SBI Swansea University Another institution paid the OA fee MR/S026193/1/MRC_/Medical Research Council/United Kingdom, MC_UU_12012/1/MRC_/Medical Research Council/United Kingdom, WT_/Wellcome Trust/United Kingdom, MC_UU_00014/1/MRC_/Medical Research Council/United Kingdom, MC_UU_12012/5/MRC_/Medical Research Council/United Kingdom. 2024-04-03T16:08:57.2672471 2023-12-04T10:18:27.5463291 Faculty of Science and Engineering School of Biosciences, Geography and Physics - Biosciences Marie T. Dittmann 0000-0002-0470-5580 1 Gabriella Lakatos 2 Jodie F. Wainwright 0009-0004-1726-2442 3 Jacek Mokrosinski 4 Eloise Cross 0000-0002-9982-8056 5 I. Sadaf Farooqi 6 Natalie J. Wallis 0000-0001-9543-3711 7 Lewis G. Halsey 0000-0002-0786-7585 8 Rory Wilson 0000-0003-3177-0177 9 Stephen O’Rahilly 0000-0003-2199-4449 10 Giles S.H. Yeo 0000-0001-8823-3615 11 Eleanor Raffan 0000-0002-1403-3538 12 65193__29898__ac2336ceb4b14321928b4a3e44fddaab.pdf 65193.VOR.pdf 2024-04-03T15:57:59.7952096 Output 1259391 application/pdf Version of Record true Distributed under the terms of a Creative Commons Attribution CC-BY licence. true eng https://creativecommons.org/licenses/by/4.0/
title Low resting metabolic rate and increased hunger due to β-MSH and β-endorphin deletion in a canine model
spellingShingle Low resting metabolic rate and increased hunger due to β-MSH and β-endorphin deletion in a canine model
Rory Wilson
title_short Low resting metabolic rate and increased hunger due to β-MSH and β-endorphin deletion in a canine model
title_full Low resting metabolic rate and increased hunger due to β-MSH and β-endorphin deletion in a canine model
title_fullStr Low resting metabolic rate and increased hunger due to β-MSH and β-endorphin deletion in a canine model
title_full_unstemmed Low resting metabolic rate and increased hunger due to β-MSH and β-endorphin deletion in a canine model
title_sort Low resting metabolic rate and increased hunger due to β-MSH and β-endorphin deletion in a canine model
author_id_str_mv 017bc6dd155098860945dc6249c4e9bc
author_id_fullname_str_mv 017bc6dd155098860945dc6249c4e9bc_***_Rory Wilson
author Rory Wilson
author2 Marie T. Dittmann
Gabriella Lakatos
Jodie F. Wainwright
Jacek Mokrosinski
Eloise Cross
I. Sadaf Farooqi
Natalie J. Wallis
Lewis G. Halsey
Rory Wilson
Stephen O’Rahilly
Giles S.H. Yeo
Eleanor Raffan
format Journal article
container_title Science Advances
container_volume 10
container_issue 10
publishDate 2024
institution Swansea University
issn 2375-2548
doi_str_mv 10.1126/sciadv.adj3823
publisher American Association for the Advancement of Science (AAAS)
college_str Faculty of Science and Engineering
hierarchytype
hierarchy_top_id facultyofscienceandengineering
hierarchy_top_title Faculty of Science and Engineering
hierarchy_parent_id facultyofscienceandengineering
hierarchy_parent_title Faculty of Science and Engineering
department_str School of Biosciences, Geography and Physics - Biosciences{{{_:::_}}}Faculty of Science and Engineering{{{_:::_}}}School of Biosciences, Geography and Physics - Biosciences
url http://dx.doi.org/10.1126/sciadv.adj3823
document_store_str 1
active_str 0
description Mutations that perturb leptin-melanocortin signaling are known to cause hyperphagia and obesity, but energy expenditure has not been well studied outside rodents. We report on a common canine mutation in pro-opiomelanocortin (POMC), which prevents production of β–melanocyte-stimulating hormone (β-MSH) and β-endorphin but not α-MSH; humans, similar to dogs, produce α-MSH and β-MSH from the POMC propeptide, but rodents produce only α-MSH. We show that energy expenditure is markedly lower in affected dogs, which also have increased motivational salience in response to a food cue, indicating increased wanting or hunger. There was no difference in satiety at a modified ad libitum meal or in their hedonic response to food, nor disruption of adrenocorticotropic hormone (ACTH) or thyroid axes. In vitro, we show that β-MSH signals comparably to α-MSH at melanocortin receptors. These data implicate β-MSH and β-endorphin as important in determining hunger and moderating energy expenditure and suggest that this role is independent of the presence of α-MSH.
published_date 2024-03-08T16:08:53Z
_version_ 1795326669233324032
score 11.012678