Chronic Uridine Administration Induces Fatty Liver and Pre-Diabetic Conditions in Mice
Uridine is a pyrimidine nucleoside that exerts restorative functions in tissues under stress. Short-term co-administration of uridine with multiple unrelated drugs prevents drug-induced liver lipid accumulation. Uridine has the ability to modulate liver metabolism; however, the precise mechanism has...
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| Veröffentlicht in: | PloS one 2016-01, Vol.11 (1), p.e0146994-e0146994 |
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| creator | Urasaki, Yasuyo Pizzorno, Giuseppe Le, Thuc T |
| description | Uridine is a pyrimidine nucleoside that exerts restorative functions in tissues under stress. Short-term co-administration of uridine with multiple unrelated drugs prevents drug-induced liver lipid accumulation. Uridine has the ability to modulate liver metabolism; however, the precise mechanism has not been delineated. In this study, long-term effects of uridine on liver metabolism were examined in both HepG2 cell cultures and C57BL/6J mice. We report that uridine administration was associated with O-GlcNAc modification of FOXO1, increased gluconeogenesis, reduced insulin signaling activity, and reduced expression of a liver-specific fatty acid binding protein FABP1. Long-term uridine feeding induced systemic glucose intolerance and severe liver lipid accumulation in mice. Our findings suggest that the therapeutic potentials of uridine should be designed for short-term acute administration. |
| doi_str_mv | 10.1371/journal.pone.0146994 |
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Short-term co-administration of uridine with multiple unrelated drugs prevents drug-induced liver lipid accumulation. Uridine has the ability to modulate liver metabolism; however, the precise mechanism has not been delineated. In this study, long-term effects of uridine on liver metabolism were examined in both HepG2 cell cultures and C57BL/6J mice. We report that uridine administration was associated with O-GlcNAc modification of FOXO1, increased gluconeogenesis, reduced insulin signaling activity, and reduced expression of a liver-specific fatty acid binding protein FABP1. Long-term uridine feeding induced systemic glucose intolerance and severe liver lipid accumulation in mice. Our findings suggest that the therapeutic potentials of uridine should be designed for short-term acute administration.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0146994</identifier><identifier>PMID: 26789264</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Accumulation ; Animal tissues ; Animals ; Biosynthesis ; Cancer ; Care and treatment ; Diabetes ; Diabetes mellitus ; Diabetic neuropathy ; Drugs ; Fatty acid-binding protein ; Fatty acids ; Fatty liver ; Fatty Liver - chemically induced ; Fatty Liver - metabolism ; Fatty Liver - pathology ; Forkhead Box Protein O1 ; Forkhead Transcription Factors - metabolism ; FOXO1 protein ; Gluconeogenesis ; Gluconeogenesis - drug effects ; Glucose Intolerance - chemically induced ; Glucose Intolerance - metabolism ; Glucose Intolerance - pathology ; Glucose tolerance ; Health sciences ; Hep G2 Cells ; Humans ; Immunoglobulins ; Insulin ; Insulin resistance ; Intolerance ; Laboratory animals ; Lipids ; Liver ; Liver diseases ; Long-term effects ; Metabolism ; Mice ; Microscopy ; Phosphorylation ; Prediabetic state ; Prediabetic State - chemically induced ; Prediabetic State - metabolism ; Prediabetic State - pathology ; Proteins ; Rodents ; Signaling ; Uridine ; Uridine - adverse effects ; Uridine - pharmacology</subject><ispartof>PloS one, 2016-01, Vol.11 (1), p.e0146994-e0146994</ispartof><rights>COPYRIGHT 2016 Public Library of Science</rights><rights>2016 Urasaki et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2016 Urasaki et al 2016 Urasaki et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-424bc6f529e87721cde9bfe67e5c9bb7a4c6cf45b85c043465b8a532eecbf0cf3</citedby><cites>FETCH-LOGICAL-c692t-424bc6f529e87721cde9bfe67e5c9bb7a4c6cf45b85c043465b8a532eecbf0cf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4720477/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4720477/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2101,2927,23865,27923,27924,53790,53792,79371,79372</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26789264$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Zhang, Yanqiao</contributor><creatorcontrib>Urasaki, Yasuyo</creatorcontrib><creatorcontrib>Pizzorno, Giuseppe</creatorcontrib><creatorcontrib>Le, Thuc T</creatorcontrib><title>Chronic Uridine Administration Induces Fatty Liver and Pre-Diabetic Conditions in Mice</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Uridine is a pyrimidine nucleoside that exerts restorative functions in tissues under stress. Short-term co-administration of uridine with multiple unrelated drugs prevents drug-induced liver lipid accumulation. Uridine has the ability to modulate liver metabolism; however, the precise mechanism has not been delineated. In this study, long-term effects of uridine on liver metabolism were examined in both HepG2 cell cultures and C57BL/6J mice. We report that uridine administration was associated with O-GlcNAc modification of FOXO1, increased gluconeogenesis, reduced insulin signaling activity, and reduced expression of a liver-specific fatty acid binding protein FABP1. Long-term uridine feeding induced systemic glucose intolerance and severe liver lipid accumulation in mice. Our findings suggest that the therapeutic potentials of uridine should be designed for short-term acute administration.</description><subject>Accumulation</subject><subject>Animal tissues</subject><subject>Animals</subject><subject>Biosynthesis</subject><subject>Cancer</subject><subject>Care and treatment</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetic neuropathy</subject><subject>Drugs</subject><subject>Fatty acid-binding protein</subject><subject>Fatty acids</subject><subject>Fatty liver</subject><subject>Fatty Liver - chemically induced</subject><subject>Fatty Liver - metabolism</subject><subject>Fatty Liver - pathology</subject><subject>Forkhead Box Protein O1</subject><subject>Forkhead Transcription Factors - metabolism</subject><subject>FOXO1 protein</subject><subject>Gluconeogenesis</subject><subject>Gluconeogenesis - drug effects</subject><subject>Glucose Intolerance - chemically induced</subject><subject>Glucose Intolerance - metabolism</subject><subject>Glucose Intolerance - 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chemically induced</topic><topic>Fatty Liver - metabolism</topic><topic>Fatty Liver - pathology</topic><topic>Forkhead Box Protein O1</topic><topic>Forkhead Transcription Factors - metabolism</topic><topic>FOXO1 protein</topic><topic>Gluconeogenesis</topic><topic>Gluconeogenesis - drug effects</topic><topic>Glucose Intolerance - chemically induced</topic><topic>Glucose Intolerance - metabolism</topic><topic>Glucose Intolerance - pathology</topic><topic>Glucose tolerance</topic><topic>Health sciences</topic><topic>Hep G2 Cells</topic><topic>Humans</topic><topic>Immunoglobulins</topic><topic>Insulin</topic><topic>Insulin resistance</topic><topic>Intolerance</topic><topic>Laboratory animals</topic><topic>Lipids</topic><topic>Liver</topic><topic>Liver diseases</topic><topic>Long-term effects</topic><topic>Metabolism</topic><topic>Mice</topic><topic>Microscopy</topic><topic>Phosphorylation</topic><topic>Prediabetic state</topic><topic>Prediabetic State - chemically induced</topic><topic>Prediabetic State - metabolism</topic><topic>Prediabetic State - pathology</topic><topic>Proteins</topic><topic>Rodents</topic><topic>Signaling</topic><topic>Uridine</topic><topic>Uridine - adverse effects</topic><topic>Uridine - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Urasaki, Yasuyo</creatorcontrib><creatorcontrib>Pizzorno, Giuseppe</creatorcontrib><creatorcontrib>Le, Thuc T</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection (ProQuest)</collection><collection>Natural Science Collection (ProQuest)</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Urasaki, Yasuyo</au><au>Pizzorno, Giuseppe</au><au>Le, Thuc T</au><au>Zhang, Yanqiao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chronic Uridine Administration Induces Fatty Liver and Pre-Diabetic Conditions in Mice</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2016-01-20</date><risdate>2016</risdate><volume>11</volume><issue>1</issue><spage>e0146994</spage><epage>e0146994</epage><pages>e0146994-e0146994</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Uridine is a pyrimidine nucleoside that exerts restorative functions in tissues under stress. Short-term co-administration of uridine with multiple unrelated drugs prevents drug-induced liver lipid accumulation. Uridine has the ability to modulate liver metabolism; however, the precise mechanism has not been delineated. In this study, long-term effects of uridine on liver metabolism were examined in both HepG2 cell cultures and C57BL/6J mice. We report that uridine administration was associated with O-GlcNAc modification of FOXO1, increased gluconeogenesis, reduced insulin signaling activity, and reduced expression of a liver-specific fatty acid binding protein FABP1. Long-term uridine feeding induced systemic glucose intolerance and severe liver lipid accumulation in mice. Our findings suggest that the therapeutic potentials of uridine should be designed for short-term acute administration.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>26789264</pmid><doi>10.1371/journal.pone.0146994</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Accumulation Animal tissues Animals Biosynthesis Cancer Care and treatment Diabetes Diabetes mellitus Diabetic neuropathy Drugs Fatty acid-binding protein Fatty acids Fatty liver Fatty Liver - chemically induced Fatty Liver - metabolism Fatty Liver - pathology Forkhead Box Protein O1 Forkhead Transcription Factors - metabolism FOXO1 protein Gluconeogenesis Gluconeogenesis - drug effects Glucose Intolerance - chemically induced Glucose Intolerance - metabolism Glucose Intolerance - pathology Glucose tolerance Health sciences Hep G2 Cells Humans Immunoglobulins Insulin Insulin resistance Intolerance Laboratory animals Lipids Liver Liver diseases Long-term effects Metabolism Mice Microscopy Phosphorylation Prediabetic state Prediabetic State - chemically induced Prediabetic State - metabolism Prediabetic State - pathology Proteins Rodents Signaling Uridine Uridine - adverse effects Uridine - pharmacology |
| title | Chronic Uridine Administration Induces Fatty Liver and Pre-Diabetic Conditions in Mice |
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