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Matriptase-2 deficiency protects from obesity by modulating iron homeostasis
Alterations in iron status have frequently been associated with obesity and other metabolic disorders. The hormone hepcidin stands out as a key regulator in the maintenance of iron homeostasis by controlling the main iron exporter, ferroportin. Here we demonstrate that the deficiency in the hepcidin...
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| Published in: | Nature communications 2018-04, Vol.9 (1), p.1350-12, Article 1350 |
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| creator | Folgueras, Alicia R. Freitas-Rodríguez, Sandra Ramsay, Andrew J. Garabaya, Cecilia Rodríguez, Francisco Velasco, Gloria López-Otín, Carlos |
| description | Alterations in iron status have frequently been associated with obesity and other metabolic disorders. The hormone hepcidin stands out as a key regulator in the maintenance of iron homeostasis by controlling the main iron exporter, ferroportin. Here we demonstrate that the deficiency in the hepcidin repressor matriptase-2 (Tmprss6) protects from high-fat diet-induced obesity.
Tmprss6
−/−
mice show a significant decrease in body fat, improved glucose tolerance and insulin sensitivity, and are protected against hepatic steatosis. Moreover, these mice exhibit a significant increase in fat lipolysis, consistent with their dramatic reduction in adiposity. Rescue experiments that block hepcidin up-regulation and restore iron levels in
Tmprss6
−/
−
mice via anti-hemojuvelin (HJV) therapy, revert the obesity-resistant phenotype of
Tmprss6
−/
−
mice. Overall, this study describes a role for matritpase-2 and hepcidin in obesity and highlights the relevance of iron regulation in the control of adipose tissue function.
Iron homeostasis dysfunctions have been associated with several metabolic disorders including obesity, steatosis and diabetes. Here the authors demonstrate that the hepcidin repressor matriptase-2 regulates adiposity and its deficiency protects mice against obesity and promotes lipolysis. |
| doi_str_mv | 10.1038/s41467-018-03853-1 |
| format | article |
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Tmprss6
−/−
mice show a significant decrease in body fat, improved glucose tolerance and insulin sensitivity, and are protected against hepatic steatosis. Moreover, these mice exhibit a significant increase in fat lipolysis, consistent with their dramatic reduction in adiposity. Rescue experiments that block hepcidin up-regulation and restore iron levels in
Tmprss6
−/
−
mice via anti-hemojuvelin (HJV) therapy, revert the obesity-resistant phenotype of
Tmprss6
−/
−
mice. Overall, this study describes a role for matritpase-2 and hepcidin in obesity and highlights the relevance of iron regulation in the control of adipose tissue function.
Iron homeostasis dysfunctions have been associated with several metabolic disorders including obesity, steatosis and diabetes. Here the authors demonstrate that the hepcidin repressor matriptase-2 regulates adiposity and its deficiency protects mice against obesity and promotes lipolysis.</description><identifier>ISSN: 2041-1723</identifier><identifier>EISSN: 2041-1723</identifier><identifier>DOI: 10.1038/s41467-018-03853-1</identifier><identifier>PMID: 29636509</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/1 ; 45/77 ; 45/90 ; 631/443/319/2723 ; 64/60 ; 692/163/2743/2037 ; 82/29 ; Adipose tissue ; Body fat ; Control ; Fatty liver ; Glucose tolerance ; Hepcidin ; High fat diet ; Homeostasis ; Humanities and Social Sciences ; Insulin ; Iron ; Lipolysis ; Metabolic disorders ; Mice ; multidisciplinary ; Obesity ; Phenotypes ; Rodents ; Science ; Science (multidisciplinary) ; Steatosis</subject><ispartof>Nature communications, 2018-04, Vol.9 (1), p.1350-12, Article 1350</ispartof><rights>The Author(s) 2018</rights><rights>2018. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c606t-ab8678e12938708388634e7706c913a4ca84550393f3de3617031eb88c61a4913</citedby><cites>FETCH-LOGICAL-c606t-ab8678e12938708388634e7706c913a4ca84550393f3de3617031eb88c61a4913</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2023717772/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2023717772?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29636509$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Folgueras, Alicia R.</creatorcontrib><creatorcontrib>Freitas-Rodríguez, Sandra</creatorcontrib><creatorcontrib>Ramsay, Andrew J.</creatorcontrib><creatorcontrib>Garabaya, Cecilia</creatorcontrib><creatorcontrib>Rodríguez, Francisco</creatorcontrib><creatorcontrib>Velasco, Gloria</creatorcontrib><creatorcontrib>López-Otín, Carlos</creatorcontrib><title>Matriptase-2 deficiency protects from obesity by modulating iron homeostasis</title><title>Nature communications</title><addtitle>Nat Commun</addtitle><addtitle>Nat Commun</addtitle><description>Alterations in iron status have frequently been associated with obesity and other metabolic disorders. The hormone hepcidin stands out as a key regulator in the maintenance of iron homeostasis by controlling the main iron exporter, ferroportin. Here we demonstrate that the deficiency in the hepcidin repressor matriptase-2 (Tmprss6) protects from high-fat diet-induced obesity.
Tmprss6
−/−
mice show a significant decrease in body fat, improved glucose tolerance and insulin sensitivity, and are protected against hepatic steatosis. Moreover, these mice exhibit a significant increase in fat lipolysis, consistent with their dramatic reduction in adiposity. Rescue experiments that block hepcidin up-regulation and restore iron levels in
Tmprss6
−/
−
mice via anti-hemojuvelin (HJV) therapy, revert the obesity-resistant phenotype of
Tmprss6
−/
−
mice. Overall, this study describes a role for matritpase-2 and hepcidin in obesity and highlights the relevance of iron regulation in the control of adipose tissue function.
Iron homeostasis dysfunctions have been associated with several metabolic disorders including obesity, steatosis and diabetes. Here the authors demonstrate that the hepcidin repressor matriptase-2 regulates adiposity and its deficiency protects mice against obesity and promotes lipolysis.</description><subject>13/1</subject><subject>45/77</subject><subject>45/90</subject><subject>631/443/319/2723</subject><subject>64/60</subject><subject>692/163/2743/2037</subject><subject>82/29</subject><subject>Adipose tissue</subject><subject>Body fat</subject><subject>Control</subject><subject>Fatty liver</subject><subject>Glucose tolerance</subject><subject>Hepcidin</subject><subject>High fat diet</subject><subject>Homeostasis</subject><subject>Humanities and Social Sciences</subject><subject>Insulin</subject><subject>Iron</subject><subject>Lipolysis</subject><subject>Metabolic disorders</subject><subject>Mice</subject><subject>multidisciplinary</subject><subject>Obesity</subject><subject>Phenotypes</subject><subject>Rodents</subject><subject>Science</subject><subject>Science 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Abstracts</collection><collection>Environment Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Nature communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Folgueras, Alicia R.</au><au>Freitas-Rodríguez, Sandra</au><au>Ramsay, Andrew J.</au><au>Garabaya, Cecilia</au><au>Rodríguez, Francisco</au><au>Velasco, Gloria</au><au>López-Otín, Carlos</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Matriptase-2 deficiency protects from obesity by modulating iron homeostasis</atitle><jtitle>Nature communications</jtitle><stitle>Nat Commun</stitle><addtitle>Nat Commun</addtitle><date>2018-04-10</date><risdate>2018</risdate><volume>9</volume><issue>1</issue><spage>1350</spage><epage>12</epage><pages>1350-12</pages><artnum>1350</artnum><issn>2041-1723</issn><eissn>2041-1723</eissn><abstract>Alterations in iron status have frequently been associated with obesity and other metabolic disorders. The hormone hepcidin stands out as a key regulator in the maintenance of iron homeostasis by controlling the main iron exporter, ferroportin. Here we demonstrate that the deficiency in the hepcidin repressor matriptase-2 (Tmprss6) protects from high-fat diet-induced obesity.
Tmprss6
−/−
mice show a significant decrease in body fat, improved glucose tolerance and insulin sensitivity, and are protected against hepatic steatosis. Moreover, these mice exhibit a significant increase in fat lipolysis, consistent with their dramatic reduction in adiposity. Rescue experiments that block hepcidin up-regulation and restore iron levels in
Tmprss6
−/
−
mice via anti-hemojuvelin (HJV) therapy, revert the obesity-resistant phenotype of
Tmprss6
−/
−
mice. Overall, this study describes a role for matritpase-2 and hepcidin in obesity and highlights the relevance of iron regulation in the control of adipose tissue function.
Iron homeostasis dysfunctions have been associated with several metabolic disorders including obesity, steatosis and diabetes. Here the authors demonstrate that the hepcidin repressor matriptase-2 regulates adiposity and its deficiency protects mice against obesity and promotes lipolysis.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>29636509</pmid><doi>10.1038/s41467-018-03853-1</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| source | Open Access: PubMed Central; Publicly Available Content Database; Springer Nature - nature.com Journals - Fully Open Access; North East Research Libraries Nature Academic Titles |
| subjects | 13/1 45/77 45/90 631/443/319/2723 64/60 692/163/2743/2037 82/29 Adipose tissue Body fat Control Fatty liver Glucose tolerance Hepcidin High fat diet Homeostasis Humanities and Social Sciences Insulin Iron Lipolysis Metabolic disorders Mice multidisciplinary Obesity Phenotypes Rodents Science Science (multidisciplinary) Steatosis |
| title | Matriptase-2 deficiency protects from obesity by modulating iron homeostasis |
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