Circadian clocks and feeding time regulate the oscillations and levels of hepatic triglycerides
Identifieur interne : 002C93 ( Ncbi/Curation ); précédent : 002C92; suivant : 002C94Circadian clocks and feeding time regulate the oscillations and levels of hepatic triglycerides
Auteurs : Yaarit Adamovich [Israël] ; Liat Rousso-Noori [Israël] ; Ziv Zwighaft [Israël] ; Adi Neufeld-Cohen [Israël] ; Marina Golik [Israël] ; Judith Kraut-Cohen [Israël] ; Miao Wang [États-Unis] ; Xianlin Han [États-Unis] ; Gad Asher [Israël]Source :
- Cell metabolism [ 1550-4131 ] ; 2014.
Abstract
Circadian clocks play a major role in orchestrating daily physiology, and their disruption can evoke metabolic diseases such as fatty liver and obesity. To study the role of circadian clocks in lipid homeostasis, we performed an extensive lipidomic analysis of liver tissues from wild type and clock-disrupted mice, fed either ad libitum or night fed. To our surprise, a similar fraction of lipids (~17%) oscillated in both mouse strains, most notably triglycerides, but with completely different phases. Moreover, several master lipid regulators (e.g. PPARα) and enzymes involved in triglyceride metabolism retained their circadian expression in clock-disrupted mice. Nighttime restricted feeding shifted the phase of triglyceride accumulation and resulted in ~50% decrease in hepatic triglyceride levels in wild type mice. Our findings suggest that circadian clocks and feeding time dictate the phase and levels of hepatic triglyceride accumulation, however oscillations in triglycerides can persist in the absence of a functional clock.
Url:
DOI: 10.1016/j.cmet.2013.12.016
PubMed: 24506873
PubMed Central: 4261230
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Chemistry, Weizmann Institute of Science, Rehovot 76100</wicri:regionArea><wicri:noRegion>Rehovot 76100</wicri:noRegion></affiliation></author><author><name sortKey="Rousso Noori, Liat" sort="Rousso Noori, Liat" uniqKey="Rousso Noori L" first="Liat" last="Rousso-Noori">Liat Rousso-Noori</name><affiliation wicri:level="1"><nlm:aff id="A1">Department of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100, Israel</nlm:aff><country xml:lang="fr">Israël</country><wicri:regionArea>Department of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100</wicri:regionArea><wicri:noRegion>Rehovot 76100</wicri:noRegion></affiliation></author><author><name sortKey="Zwighaft, Ziv" sort="Zwighaft, Ziv" uniqKey="Zwighaft Z" first="Ziv" last="Zwighaft">Ziv Zwighaft</name><affiliation wicri:level="1"><nlm:aff id="A1">Department of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100, Israel</nlm:aff><country xml:lang="fr">Israël</country><wicri:regionArea>Department of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100</wicri:regionArea><wicri:noRegion>Rehovot 76100</wicri:noRegion></affiliation></author><author><name sortKey="Neufeld Cohen, Adi" sort="Neufeld Cohen, Adi" uniqKey="Neufeld Cohen A" first="Adi" last="Neufeld-Cohen">Adi Neufeld-Cohen</name><affiliation wicri:level="1"><nlm:aff id="A1">Department of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100, Israel</nlm:aff><country xml:lang="fr">Israël</country><wicri:regionArea>Department of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100</wicri:regionArea><wicri:noRegion>Rehovot 76100</wicri:noRegion></affiliation></author><author><name sortKey="Golik, Marina" sort="Golik, Marina" uniqKey="Golik M" first="Marina" last="Golik">Marina Golik</name><affiliation wicri:level="1"><nlm:aff id="A1">Department of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100, Israel</nlm:aff><country xml:lang="fr">Israël</country><wicri:regionArea>Department of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100</wicri:regionArea><wicri:noRegion>Rehovot 76100</wicri:noRegion></affiliation></author><author><name sortKey="Kraut Cohen, Judith" sort="Kraut Cohen, Judith" uniqKey="Kraut Cohen J" first="Judith" last="Kraut-Cohen">Judith Kraut-Cohen</name><affiliation wicri:level="1"><nlm:aff id="A1">Department of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100, Israel</nlm:aff><country xml:lang="fr">Israël</country><wicri:regionArea>Department of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100</wicri:regionArea><wicri:noRegion>Rehovot 76100</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Miao" sort="Wang, Miao" uniqKey="Wang M" first="Miao" last="Wang">Miao Wang</name><affiliation wicri:level="2"><nlm:aff id="A2">Diabetes and Obesity Research Center, Sanford-Burnham Medical Research Institute, Orlando, FL 32827, U.S.A</nlm:aff><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea>Diabetes and Obesity Research Center, Sanford-Burnham Medical Research Institute, Orlando, FL 32827</wicri:regionArea><placeName><region type="state">Floride</region></placeName></affiliation></author><author><name sortKey="Han, Xianlin" sort="Han, Xianlin" uniqKey="Han X" first="Xianlin" last="Han">Xianlin Han</name><affiliation wicri:level="2"><nlm:aff id="A2">Diabetes and Obesity Research Center, Sanford-Burnham Medical Research Institute, Orlando, FL 32827, U.S.A</nlm:aff><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea>Diabetes and Obesity Research Center, Sanford-Burnham Medical Research Institute, Orlando, FL 32827</wicri:regionArea><placeName><region type="state">Floride</region></placeName></affiliation></author><author><name sortKey="Asher, Gad" sort="Asher, Gad" uniqKey="Asher G" first="Gad" last="Asher">Gad Asher</name><affiliation wicri:level="1"><nlm:aff id="A1">Department of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100, Israel</nlm:aff><country xml:lang="fr">Israël</country><wicri:regionArea>Department of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100</wicri:regionArea><wicri:noRegion>Rehovot 76100</wicri:noRegion></affiliation></author></analytic><series><title level="j">Cell metabolism</title><idno type="ISSN">1550-4131</idno><idno type="eISSN">1932-7420</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><title>Summary</title><p id="P2">Circadian clocks play a major role in orchestrating daily physiology, and their disruption can evoke metabolic diseases such as fatty liver and obesity. To study the role of circadian clocks in lipid homeostasis, we performed an extensive lipidomic analysis of liver tissues from wild type and clock-disrupted mice, fed either ad libitum or night fed. To our surprise, a similar fraction of lipids (~17%) oscillated in both mouse strains, most notably triglycerides, but with completely different phases. Moreover, several master lipid regulators (e.g. PPARα) and enzymes involved in triglyceride metabolism retained their circadian expression in clock-disrupted mice. Nighttime restricted feeding shifted the phase of triglyceride accumulation and resulted in ~50% decrease in hepatic triglyceride levels in wild type mice. Our findings suggest that circadian clocks and feeding time dictate the phase and levels of hepatic triglyceride accumulation, however oscillations in triglycerides can persist in the absence of a functional clock.</p></div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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