The Deubiquitinase OTUB1 Is a Key Regulator of Energy Metabolism
Dysregulated energy metabolism is a major contributor to a multitude of pathologies, including obesity and diabetes. Understanding the regulation of metabolic homeostasis is of utmost importance for the identification of therapeutic targets for the treatment of metabolically driven diseases. We prev...
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| Veröffentlicht in: | International journal of molecular sciences 2022-01, Vol.23 (3), p.1536 |
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| creator | Ruiz-Serrano, Amalia Boyle, Christina N Monné Rodríguez, Josep M Günter, Julia Jucht, Agnieszka E Pfundstein, Svende Bapst, Andreas M Lutz, Thomas A Wenger, Roland H Scholz, Carsten C |
| description | Dysregulated energy metabolism is a major contributor to a multitude of pathologies, including obesity and diabetes. Understanding the regulation of metabolic homeostasis is of utmost importance for the identification of therapeutic targets for the treatment of metabolically driven diseases. We previously identified the deubiquitinase OTUB1 as substrate for the cellular oxygen sensor factor-inhibiting HIF (FIH) with regulatory effects on cellular energy metabolism, but the physiological relevance of OTUB1 is unclear. Here, we report that the induced global deletion of OTUB1 in adult mice (
iKO) elevated energy expenditure, reduced age-dependent body weight gain, facilitated blood glucose clearance and lowered basal plasma insulin levels. The respiratory exchange ratio was maintained, indicating an unaltered nutrient oxidation. In addition,
deletion in cells enhanced AKT activity, leading to a larger cell size, higher ATP levels and reduced AMPK phosphorylation. AKT is an integral part of insulin-mediated signaling and
iKO mice presented with increased AKT phosphorylation following acute insulin administration combined with insulin hypersensitivity. We conclude that OTUB1 is an important regulator of metabolic homeostasis. |
| doi_str_mv | 10.3390/ijms23031536 |
| format | Article |
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iKO) elevated energy expenditure, reduced age-dependent body weight gain, facilitated blood glucose clearance and lowered basal plasma insulin levels. The respiratory exchange ratio was maintained, indicating an unaltered nutrient oxidation. In addition,
deletion in cells enhanced AKT activity, leading to a larger cell size, higher ATP levels and reduced AMPK phosphorylation. AKT is an integral part of insulin-mediated signaling and
iKO mice presented with increased AKT phosphorylation following acute insulin administration combined with insulin hypersensitivity. We conclude that OTUB1 is an important regulator of metabolic homeostasis.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms23031536</identifier><identifier>PMID: 35163456</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Adenosine Triphosphate - metabolism ; Adenylate Kinase - metabolism ; AKT protein ; Amino acids ; Animals ; Blood Glucose ; Body fat ; Body Weight ; Body weight gain ; Cell Size ; Cells, Cultured ; Clonal deletion ; Cysteine Endopeptidases - genetics ; Cysteine Endopeptidases - metabolism ; Diabetes mellitus ; Energy ; Energy expenditure ; Energy Metabolism ; Fibroblasts - cytology ; Fibroblasts - drug effects ; Fibroblasts - metabolism ; Gene Deletion ; Genotype & phenotype ; Glucose ; Homeostasis ; Hypersensitivity ; Hyperthyroidism ; Insulin ; Insulin - administration & dosage ; Insulin - adverse effects ; Insulin Resistance - genetics ; Kinases ; Metabolism ; Mice ; Mixed Function Oxygenases - metabolism ; Oxidation ; Oxygen probes ; Phosphorylation ; Physiological effects ; Proteins ; Proto-Oncogene Proteins c-akt - metabolism ; Therapeutic targets ; Thyroid gland</subject><ispartof>International journal of molecular sciences, 2022-01, Vol.23 (3), p.1536</ispartof><rights>2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022 by the authors. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c412t-7e4d739d19407687d37ee5beb67c9254765d73d14304dabacd58ae75452d48903</citedby><cites>FETCH-LOGICAL-c412t-7e4d739d19407687d37ee5beb67c9254765d73d14304dabacd58ae75452d48903</cites><orcidid>0000-0002-5056-8548 ; 0000-0002-4553-4319 ; 0000-0001-6579-8015 ; 0000-0001-7592-4839 ; 0000-0002-1060-2529 ; 0000-0002-2574-0780 ; 0000-0002-9397-5653</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8836018/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8836018/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35163456$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ruiz-Serrano, Amalia</creatorcontrib><creatorcontrib>Boyle, Christina N</creatorcontrib><creatorcontrib>Monné Rodríguez, Josep M</creatorcontrib><creatorcontrib>Günter, Julia</creatorcontrib><creatorcontrib>Jucht, Agnieszka E</creatorcontrib><creatorcontrib>Pfundstein, Svende</creatorcontrib><creatorcontrib>Bapst, Andreas M</creatorcontrib><creatorcontrib>Lutz, Thomas A</creatorcontrib><creatorcontrib>Wenger, Roland H</creatorcontrib><creatorcontrib>Scholz, Carsten C</creatorcontrib><title>The Deubiquitinase OTUB1 Is a Key Regulator of Energy Metabolism</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Dysregulated energy metabolism is a major contributor to a multitude of pathologies, including obesity and diabetes. Understanding the regulation of metabolic homeostasis is of utmost importance for the identification of therapeutic targets for the treatment of metabolically driven diseases. We previously identified the deubiquitinase OTUB1 as substrate for the cellular oxygen sensor factor-inhibiting HIF (FIH) with regulatory effects on cellular energy metabolism, but the physiological relevance of OTUB1 is unclear. Here, we report that the induced global deletion of OTUB1 in adult mice (
iKO) elevated energy expenditure, reduced age-dependent body weight gain, facilitated blood glucose clearance and lowered basal plasma insulin levels. The respiratory exchange ratio was maintained, indicating an unaltered nutrient oxidation. In addition,
deletion in cells enhanced AKT activity, leading to a larger cell size, higher ATP levels and reduced AMPK phosphorylation. AKT is an integral part of insulin-mediated signaling and
iKO mice presented with increased AKT phosphorylation following acute insulin administration combined with insulin hypersensitivity. We conclude that OTUB1 is an important regulator of metabolic homeostasis.</description><subject>Adenosine Triphosphate - metabolism</subject><subject>Adenylate Kinase - metabolism</subject><subject>AKT protein</subject><subject>Amino acids</subject><subject>Animals</subject><subject>Blood Glucose</subject><subject>Body fat</subject><subject>Body Weight</subject><subject>Body weight gain</subject><subject>Cell Size</subject><subject>Cells, Cultured</subject><subject>Clonal deletion</subject><subject>Cysteine Endopeptidases - genetics</subject><subject>Cysteine Endopeptidases - metabolism</subject><subject>Diabetes mellitus</subject><subject>Energy</subject><subject>Energy expenditure</subject><subject>Energy Metabolism</subject><subject>Fibroblasts - cytology</subject><subject>Fibroblasts - drug effects</subject><subject>Fibroblasts - metabolism</subject><subject>Gene Deletion</subject><subject>Genotype & phenotype</subject><subject>Glucose</subject><subject>Homeostasis</subject><subject>Hypersensitivity</subject><subject>Hyperthyroidism</subject><subject>Insulin</subject><subject>Insulin - 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metabolism</topic><topic>Adenylate Kinase - metabolism</topic><topic>AKT protein</topic><topic>Amino acids</topic><topic>Animals</topic><topic>Blood Glucose</topic><topic>Body fat</topic><topic>Body Weight</topic><topic>Body weight gain</topic><topic>Cell Size</topic><topic>Cells, Cultured</topic><topic>Clonal deletion</topic><topic>Cysteine Endopeptidases - genetics</topic><topic>Cysteine Endopeptidases - metabolism</topic><topic>Diabetes mellitus</topic><topic>Energy</topic><topic>Energy expenditure</topic><topic>Energy Metabolism</topic><topic>Fibroblasts - cytology</topic><topic>Fibroblasts - drug effects</topic><topic>Fibroblasts - metabolism</topic><topic>Gene Deletion</topic><topic>Genotype & phenotype</topic><topic>Glucose</topic><topic>Homeostasis</topic><topic>Hypersensitivity</topic><topic>Hyperthyroidism</topic><topic>Insulin</topic><topic>Insulin - administration & dosage</topic><topic>Insulin - adverse effects</topic><topic>Insulin Resistance - genetics</topic><topic>Kinases</topic><topic>Metabolism</topic><topic>Mice</topic><topic>Mixed Function Oxygenases - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ruiz-Serrano, Amalia</au><au>Boyle, Christina N</au><au>Monné Rodríguez, Josep M</au><au>Günter, Julia</au><au>Jucht, Agnieszka E</au><au>Pfundstein, Svende</au><au>Bapst, Andreas M</au><au>Lutz, Thomas A</au><au>Wenger, Roland H</au><au>Scholz, Carsten C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Deubiquitinase OTUB1 Is a Key Regulator of Energy Metabolism</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2022-01-28</date><risdate>2022</risdate><volume>23</volume><issue>3</issue><spage>1536</spage><pages>1536-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>Dysregulated energy metabolism is a major contributor to a multitude of pathologies, including obesity and diabetes. Understanding the regulation of metabolic homeostasis is of utmost importance for the identification of therapeutic targets for the treatment of metabolically driven diseases. We previously identified the deubiquitinase OTUB1 as substrate for the cellular oxygen sensor factor-inhibiting HIF (FIH) with regulatory effects on cellular energy metabolism, but the physiological relevance of OTUB1 is unclear. Here, we report that the induced global deletion of OTUB1 in adult mice (
iKO) elevated energy expenditure, reduced age-dependent body weight gain, facilitated blood glucose clearance and lowered basal plasma insulin levels. The respiratory exchange ratio was maintained, indicating an unaltered nutrient oxidation. In addition,
deletion in cells enhanced AKT activity, leading to a larger cell size, higher ATP levels and reduced AMPK phosphorylation. AKT is an integral part of insulin-mediated signaling and
iKO mice presented with increased AKT phosphorylation following acute insulin administration combined with insulin hypersensitivity. We conclude that OTUB1 is an important regulator of metabolic homeostasis.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>35163456</pmid><doi>10.3390/ijms23031536</doi><orcidid>https://orcid.org/0000-0002-5056-8548</orcidid><orcidid>https://orcid.org/0000-0002-4553-4319</orcidid><orcidid>https://orcid.org/0000-0001-6579-8015</orcidid><orcidid>https://orcid.org/0000-0001-7592-4839</orcidid><orcidid>https://orcid.org/0000-0002-1060-2529</orcidid><orcidid>https://orcid.org/0000-0002-2574-0780</orcidid><orcidid>https://orcid.org/0000-0002-9397-5653</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | International journal of molecular sciences, 2022-01, Vol.23 (3), p.1536 |
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| source | MDPI - Multidisciplinary Digital Publishing Institute; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Adenosine Triphosphate - metabolism Adenylate Kinase - metabolism AKT protein Amino acids Animals Blood Glucose Body fat Body Weight Body weight gain Cell Size Cells, Cultured Clonal deletion Cysteine Endopeptidases - genetics Cysteine Endopeptidases - metabolism Diabetes mellitus Energy Energy expenditure Energy Metabolism Fibroblasts - cytology Fibroblasts - drug effects Fibroblasts - metabolism Gene Deletion Genotype & phenotype Glucose Homeostasis Hypersensitivity Hyperthyroidism Insulin Insulin - administration & dosage Insulin - adverse effects Insulin Resistance - genetics Kinases Metabolism Mice Mixed Function Oxygenases - metabolism Oxidation Oxygen probes Phosphorylation Physiological effects Proteins Proto-Oncogene Proteins c-akt - metabolism Therapeutic targets Thyroid gland |
| title | The Deubiquitinase OTUB1 Is a Key Regulator of Energy Metabolism |
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