Beta-lapachone, a modulator of NAD metabolism, prevents health declines in aged mice
NADH-quinone oxidoreductase 1 (NQO1) modulates cellular NAD(+)/NADH ratio which has been associated with the aging and anti-aging mechanisms of calorie restriction (CR). Here, we demonstrate that the facilitation of NQO1 activity by feeding β-lapachone (βL), an exogenous NQO1 co-substrate, prevented...
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| Veröffentlicht in: | PloS one 2012-10, Vol.7 (10), p.e47122 |
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| creator | Lee, Jeong-sook Park, Ah Hyung Lee, Sang-Hee Lee, Seoung-Hoon Kim, Jin-Hwan Yang, Suk-Jin Yeom, Young Il Kwak, Tae Hwan Lee, Dongyeop Lee, Seung-Jae Lee, Chul-Ho Kim, Jin Man Kim, Daesoo |
| description | NADH-quinone oxidoreductase 1 (NQO1) modulates cellular NAD(+)/NADH ratio which has been associated with the aging and anti-aging mechanisms of calorie restriction (CR). Here, we demonstrate that the facilitation of NQO1 activity by feeding β-lapachone (βL), an exogenous NQO1 co-substrate, prevented age-dependent decline of motor and cognitive function in aged mice. βL-fed mice did not alter their food-intake or locomotor activity but did increase their energy expenditure as measured by oxygen consumption and heat generation. Mitochondrial structure and numbers were disorganized and decreased in the muscles of control diet group but those defects were less severe in βL-fed aged mice. Furthermore, for a subset of genes associated with energy metabolism, mice fed the βL-diet showed similar changes in gene expression to the CR group (fed 70% of the control diet). These results support the potentiation of NQO1 activity by a βL diet and could be an option for preventing age-related decline of muscle and brain functions. |
| doi_str_mv | 10.1371/journal.pone.0047122 |
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Here, we demonstrate that the facilitation of NQO1 activity by feeding β-lapachone (βL), an exogenous NQO1 co-substrate, prevented age-dependent decline of motor and cognitive function in aged mice. βL-fed mice did not alter their food-intake or locomotor activity but did increase their energy expenditure as measured by oxygen consumption and heat generation. Mitochondrial structure and numbers were disorganized and decreased in the muscles of control diet group but those defects were less severe in βL-fed aged mice. Furthermore, for a subset of genes associated with energy metabolism, mice fed the βL-diet showed similar changes in gene expression to the CR group (fed 70% of the control diet). These results support the potentiation of NQO1 activity by a βL diet and could be an option for preventing age-related decline of muscle and brain functions.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0047122</identifier><identifier>PMID: 23071729</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Age ; Aging ; Aging - drug effects ; Aging - physiology ; Alzheimer's disease ; Alzheimers disease ; Animals ; Behavior, Animal - drug effects ; Biology ; Biotechnology ; Body Weight - drug effects ; Brain ; Caloric Restriction ; Cognition - drug effects ; Cognitive ability ; Diet ; Dietary Supplements ; Energy expenditure ; Energy measurement ; Energy metabolism ; Energy Metabolism - drug effects ; Experiments ; Food intake ; Gene expression ; Gene Expression Regulation - drug effects ; Genomics ; Heat generation ; Kinases ; Lapachone ; Life sciences ; Locomotor activity ; Male ; Medical research ; Medicine ; Metabolism ; Mice ; Mice, Inbred C57BL ; Mitochondria ; Mitochondria - drug effects ; Muscle, Skeletal - drug effects ; Muscles ; NAD ; NAD - metabolism ; NAD(P)H Dehydrogenase (Quinone) - metabolism ; NADH ; NADH-quinone oxidoreductase ; Naphthoquinones - pharmacology ; Nicotinamide adenine dinucleotide ; Nutrient deficiency ; Oxidoreductase ; Oxidoreductases ; Oxygen ; Oxygen consumption ; Potentiation ; Quinone ; Quinone oxidoreductase ; R&D ; Research & development ; Substrates</subject><ispartof>PloS one, 2012-10, Vol.7 (10), p.e47122</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>Lee et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://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>2012 Lee et al 2012 Lee et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-7672235544d813ee7397b3e84afc2bc4baf740aa5b8aff5440ad479ee1732ab73</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3469505/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3469505/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,2103,2929,23871,27929,27930,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23071729$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Bai, Yidong</contributor><creatorcontrib>Lee, Jeong-sook</creatorcontrib><creatorcontrib>Park, Ah Hyung</creatorcontrib><creatorcontrib>Lee, Sang-Hee</creatorcontrib><creatorcontrib>Lee, Seoung-Hoon</creatorcontrib><creatorcontrib>Kim, Jin-Hwan</creatorcontrib><creatorcontrib>Yang, Suk-Jin</creatorcontrib><creatorcontrib>Yeom, Young Il</creatorcontrib><creatorcontrib>Kwak, Tae Hwan</creatorcontrib><creatorcontrib>Lee, Dongyeop</creatorcontrib><creatorcontrib>Lee, Seung-Jae</creatorcontrib><creatorcontrib>Lee, Chul-Ho</creatorcontrib><creatorcontrib>Kim, Jin Man</creatorcontrib><creatorcontrib>Kim, Daesoo</creatorcontrib><title>Beta-lapachone, a modulator of NAD metabolism, prevents health declines in aged mice</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>NADH-quinone oxidoreductase 1 (NQO1) modulates cellular NAD(+)/NADH ratio which has been associated with the aging and anti-aging mechanisms of calorie restriction (CR). Here, we demonstrate that the facilitation of NQO1 activity by feeding β-lapachone (βL), an exogenous NQO1 co-substrate, prevented age-dependent decline of motor and cognitive function in aged mice. βL-fed mice did not alter their food-intake or locomotor activity but did increase their energy expenditure as measured by oxygen consumption and heat generation. Mitochondrial structure and numbers were disorganized and decreased in the muscles of control diet group but those defects were less severe in βL-fed aged mice. Furthermore, for a subset of genes associated with energy metabolism, mice fed the βL-diet showed similar changes in gene expression to the CR group (fed 70% of the control diet). These results support the potentiation of NQO1 activity by a βL diet and could be an option for preventing age-related decline of muscle and brain functions.</description><subject>Age</subject><subject>Aging</subject><subject>Aging - drug effects</subject><subject>Aging - physiology</subject><subject>Alzheimer's disease</subject><subject>Alzheimers disease</subject><subject>Animals</subject><subject>Behavior, Animal - drug effects</subject><subject>Biology</subject><subject>Biotechnology</subject><subject>Body Weight - drug effects</subject><subject>Brain</subject><subject>Caloric Restriction</subject><subject>Cognition - drug effects</subject><subject>Cognitive ability</subject><subject>Diet</subject><subject>Dietary Supplements</subject><subject>Energy expenditure</subject><subject>Energy measurement</subject><subject>Energy metabolism</subject><subject>Energy Metabolism - drug effects</subject><subject>Experiments</subject><subject>Food intake</subject><subject>Gene 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deficiency</subject><subject>Oxidoreductase</subject><subject>Oxidoreductases</subject><subject>Oxygen</subject><subject>Oxygen consumption</subject><subject>Potentiation</subject><subject>Quinone</subject><subject>Quinone oxidoreductase</subject><subject>R&D</subject><subject>Research & 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a modulator of NAD metabolism, prevents health declines in aged mice</title><author>Lee, Jeong-sook ; Park, Ah Hyung ; Lee, Sang-Hee ; Lee, Seoung-Hoon ; Kim, Jin-Hwan ; Yang, Suk-Jin ; Yeom, Young Il ; Kwak, Tae Hwan ; Lee, Dongyeop ; Lee, Seung-Jae ; Lee, Chul-Ho ; Kim, Jin Man ; Kim, Daesoo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-7672235544d813ee7397b3e84afc2bc4baf740aa5b8aff5440ad479ee1732ab73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Age</topic><topic>Aging</topic><topic>Aging - drug effects</topic><topic>Aging - physiology</topic><topic>Alzheimer's disease</topic><topic>Alzheimers disease</topic><topic>Animals</topic><topic>Behavior, Animal - drug effects</topic><topic>Biology</topic><topic>Biotechnology</topic><topic>Body Weight - drug effects</topic><topic>Brain</topic><topic>Caloric Restriction</topic><topic>Cognition - drug effects</topic><topic>Cognitive ability</topic><topic>Diet</topic><topic>Dietary Supplements</topic><topic>Energy expenditure</topic><topic>Energy measurement</topic><topic>Energy metabolism</topic><topic>Energy Metabolism - drug effects</topic><topic>Experiments</topic><topic>Food intake</topic><topic>Gene expression</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Genomics</topic><topic>Heat generation</topic><topic>Kinases</topic><topic>Lapachone</topic><topic>Life sciences</topic><topic>Locomotor activity</topic><topic>Male</topic><topic>Medical research</topic><topic>Medicine</topic><topic>Metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mitochondria</topic><topic>Mitochondria - drug effects</topic><topic>Muscle, Skeletal - drug effects</topic><topic>Muscles</topic><topic>NAD</topic><topic>NAD - metabolism</topic><topic>NAD(P)H Dehydrogenase (Quinone) - metabolism</topic><topic>NADH</topic><topic>NADH-quinone oxidoreductase</topic><topic>Naphthoquinones - pharmacology</topic><topic>Nicotinamide adenine dinucleotide</topic><topic>Nutrient deficiency</topic><topic>Oxidoreductase</topic><topic>Oxidoreductases</topic><topic>Oxygen</topic><topic>Oxygen consumption</topic><topic>Potentiation</topic><topic>Quinone</topic><topic>Quinone oxidoreductase</topic><topic>R&D</topic><topic>Research & development</topic><topic>Substrates</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Jeong-sook</creatorcontrib><creatorcontrib>Park, Ah Hyung</creatorcontrib><creatorcontrib>Lee, Sang-Hee</creatorcontrib><creatorcontrib>Lee, Seoung-Hoon</creatorcontrib><creatorcontrib>Kim, Jin-Hwan</creatorcontrib><creatorcontrib>Yang, Suk-Jin</creatorcontrib><creatorcontrib>Yeom, Young Il</creatorcontrib><creatorcontrib>Kwak, Tae Hwan</creatorcontrib><creatorcontrib>Lee, Dongyeop</creatorcontrib><creatorcontrib>Lee, Seung-Jae</creatorcontrib><creatorcontrib>Lee, 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Il</au><au>Kwak, Tae Hwan</au><au>Lee, Dongyeop</au><au>Lee, Seung-Jae</au><au>Lee, Chul-Ho</au><au>Kim, Jin Man</au><au>Kim, Daesoo</au><au>Bai, Yidong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Beta-lapachone, a modulator of NAD metabolism, prevents health declines in aged mice</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2012-10-11</date><risdate>2012</risdate><volume>7</volume><issue>10</issue><spage>e47122</spage><pages>e47122-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>NADH-quinone oxidoreductase 1 (NQO1) modulates cellular NAD(+)/NADH ratio which has been associated with the aging and anti-aging mechanisms of calorie restriction (CR). Here, we demonstrate that the facilitation of NQO1 activity by feeding β-lapachone (βL), an exogenous NQO1 co-substrate, prevented age-dependent decline of motor and cognitive function in aged mice. βL-fed mice did not alter their food-intake or locomotor activity but did increase their energy expenditure as measured by oxygen consumption and heat generation. Mitochondrial structure and numbers were disorganized and decreased in the muscles of control diet group but those defects were less severe in βL-fed aged mice. Furthermore, for a subset of genes associated with energy metabolism, mice fed the βL-diet showed similar changes in gene expression to the CR group (fed 70% of the control diet). These results support the potentiation of NQO1 activity by a βL diet and could be an option for preventing age-related decline of muscle and brain functions.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23071729</pmid><doi>10.1371/journal.pone.0047122</doi><tpages>e47122</tpages><oa>free_for_read</oa></addata></record> |
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| language | eng |
| recordid | cdi_plos_journals_1326559259 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS) Journals Open Access; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Age Aging Aging - drug effects Aging - physiology Alzheimer's disease Alzheimers disease Animals Behavior, Animal - drug effects Biology Biotechnology Body Weight - drug effects Brain Caloric Restriction Cognition - drug effects Cognitive ability Diet Dietary Supplements Energy expenditure Energy measurement Energy metabolism Energy Metabolism - drug effects Experiments Food intake Gene expression Gene Expression Regulation - drug effects Genomics Heat generation Kinases Lapachone Life sciences Locomotor activity Male Medical research Medicine Metabolism Mice Mice, Inbred C57BL Mitochondria Mitochondria - drug effects Muscle, Skeletal - drug effects Muscles NAD NAD - metabolism NAD(P)H Dehydrogenase (Quinone) - metabolism NADH NADH-quinone oxidoreductase Naphthoquinones - pharmacology Nicotinamide adenine dinucleotide Nutrient deficiency Oxidoreductase Oxidoreductases Oxygen Oxygen consumption Potentiation Quinone Quinone oxidoreductase R&D Research & development Substrates |
| title | Beta-lapachone, a modulator of NAD metabolism, prevents health declines in aged mice |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-15T19%3A43%3A39IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Beta-lapachone,%20a%20modulator%20of%20NAD%20metabolism,%20prevents%20health%20declines%20in%20aged%20mice&rft.jtitle=PloS%20one&rft.au=Lee,%20Jeong-sook&rft.date=2012-10-11&rft.volume=7&rft.issue=10&rft.spage=e47122&rft.pages=e47122-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0047122&rft_dat=%3Cgale_plos_%3EA498257952%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1326559259&rft_id=info:pmid/23071729&rft_galeid=A498257952&rft_doaj_id=oai_doaj_org_article_7cefc0f93dbb4d32bed0f9646c1a468c&rfr_iscdi=true |