FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2074549593> ?p ?o ?g. }

• W2074549593 endingPage "36051" @default.
• W2074549593 startingPage "36040" @default.
• W2074549593 abstract "NAT8L (N-acetyltransferase 8-like) catalyzes the formation of N-acetylaspartate (NAA) from acetyl-CoA and aspartate. In the brain, NAA delivers the acetate moiety for synthesis of acetyl-CoA that is further used for fatty acid generation. However, its function in other tissues remained elusive. Here, we show for the first time that Nat8l is highly expressed in adipose tissues and murine and human adipogenic cell lines and is localized in the mitochondria of brown adipocytes. Stable overexpression of Nat8l in immortalized brown adipogenic cells strongly increases glucose incorporation into neutral lipids, accompanied by increased lipolysis, indicating an accelerated lipid turnover. Additionally, mitochondrial mass and number as well as oxygen consumption are elevated upon Nat8l overexpression. Concordantly, expression levels of brown marker genes, such as Prdm16, Cidea, Pgc1α, Pparα, and particularly UCP1, are markedly elevated in these cells. Treatment with a PPARα antagonist indicates that the increase in UCP1 expression and oxygen consumption is PPARα-dependent. Nat8l knockdown in brown adipocytes has no impact on cellular triglyceride content, lipogenesis, or oxygen consumption, but lipolysis and brown marker gene expression are increased; the latter is also observed in BAT of Nat8l-KO mice. Interestingly, the expression of ATP-citrate lyase is increased in Nat8l-silenced adipocytes and BAT of Nat8l-KO mice, indicating a compensatory mechanism to sustain the acetyl-CoA pool once Nat8l levels are reduced. Taken together, our data show that Nat8l impacts on the brown adipogenic phenotype and suggests the existence of the NAT8L-driven NAA metabolism as a novel pathway to provide cytosolic acetyl-CoA for lipid synthesis in adipocytes. NAT8L (N-acetyltransferase 8-like) catalyzes the formation of N-acetylaspartate (NAA) from acetyl-CoA and aspartate. In the brain, NAA delivers the acetate moiety for synthesis of acetyl-CoA that is further used for fatty acid generation. However, its function in other tissues remained elusive. Here, we show for the first time that Nat8l is highly expressed in adipose tissues and murine and human adipogenic cell lines and is localized in the mitochondria of brown adipocytes. Stable overexpression of Nat8l in immortalized brown adipogenic cells strongly increases glucose incorporation into neutral lipids, accompanied by increased lipolysis, indicating an accelerated lipid turnover. Additionally, mitochondrial mass and number as well as oxygen consumption are elevated upon Nat8l overexpression. Concordantly, expression levels of brown marker genes, such as Prdm16, Cidea, Pgc1α, Pparα, and particularly UCP1, are markedly elevated in these cells. Treatment with a PPARα antagonist indicates that the increase in UCP1 expression and oxygen consumption is PPARα-dependent. Nat8l knockdown in brown adipocytes has no impact on cellular triglyceride content, lipogenesis, or oxygen consumption, but lipolysis and brown marker gene expression are increased; the latter is also observed in BAT of Nat8l-KO mice. Interestingly, the expression of ATP-citrate lyase is increased in Nat8l-silenced adipocytes and BAT of Nat8l-KO mice, indicating a compensatory mechanism to sustain the acetyl-CoA pool once Nat8l levels are reduced. Taken together, our data show that Nat8l impacts on the brown adipogenic phenotype and suggests the existence of the NAT8L-driven NAA metabolism as a novel pathway to provide cytosolic acetyl-CoA for lipid synthesis in adipocytes." @default.
• W2074549593 created "2016-06-24" @default.
• W2074549593 creator A5006128068 @default.
• W2074549593 creator A5012827429 @default.
• W2074549593 creator A5014787862 @default.
• W2074549593 creator A5018496662 @default.
• W2074549593 creator A5019361653 @default.
• W2074549593 creator A5050117572 @default.
• W2074549593 creator A5053111848 @default.
• W2074549593 creator A5060591351 @default.
• W2074549593 creator A5066477976 @default.
• W2074549593 creator A5076385970 @default.
• W2074549593 creator A5080561801 @default.
• W2074549593 creator A5088623617 @default.
• W2074549593 creator A5089686807 @default.
• W2074549593 date "2013-12-01" @default.
• W2074549593 modified "2023-10-07" @default.
• W2074549593 title "NAT8L (N-Acetyltransferase 8-Like) Accelerates Lipid Turnover and Increases Energy Expenditure in Brown Adipocytes" @default.
• W2074549593 cites W1569479994 @default.
• W2074549593 cites W1922984638 @default.
• W2074549593 cites W1965079305 @default.
• W2074549593 cites W1965392584 @default.
• W2074549593 cites W1965397552 @default.
• W2074549593 cites W1971082641 @default.
• W2074549593 cites W1974134896 @default.
• W2074549593 cites W1980722983 @default.
• W2074549593 cites W1981820664 @default.
• W2074549593 cites W1983006621 @default.
• W2074549593 cites W1987422593 @default.
• W2074549593 cites W1987849310 @default.
• W2074549593 cites W1991234756 @default.
• W2074549593 cites W1992326632 @default.
• W2074549593 cites W2005827500 @default.
• W2074549593 cites W2008632158 @default.
• W2074549593 cites W2014860237 @default.
• W2074549593 cites W2026384935 @default.
• W2074549593 cites W2031622188 @default.
• W2074549593 cites W2035343079 @default.
• W2074549593 cites W2040328785 @default.
• W2074549593 cites W2040563918 @default.
• W2074549593 cites W2044152892 @default.
• W2074549593 cites W2047306805 @default.
• W2074549593 cites W2049215659 @default.
• W2074549593 cites W2052786647 @default.
• W2074549593 cites W2055212957 @default.
• W2074549593 cites W2059580548 @default.
• W2074549593 cites W2084680375 @default.
• W2074549593 cites W2090812766 @default.
• W2074549593 cites W2091614510 @default.
• W2074549593 cites W2093103724 @default.
• W2074549593 cites W2093361250 @default.
• W2074549593 cites W2095348472 @default.
• W2074549593 cites W2095914839 @default.
• W2074549593 cites W2096842458 @default.
• W2074549593 cites W2098327516 @default.
• W2074549593 cites W2098457930 @default.
• W2074549593 cites W2110839026 @default.
• W2074549593 cites W2128565360 @default.
• W2074549593 cites W2130908205 @default.
• W2074549593 cites W2132358997 @default.
• W2074549593 cites W2132545213 @default.
• W2074549593 cites W2135345594 @default.
• W2074549593 cites W2137489081 @default.
• W2074549593 cites W2143965359 @default.
• W2074549593 cites W2148403724 @default.
• W2074549593 cites W2162023168 @default.
• W2074549593 cites W38541217 @default.
• W2074549593 cites W4238372547 @default.
• W2074549593 doi "https://doi.org/10.1074/jbc.m113.491324" @default.
• W2074549593 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3861652" @default.
• W2074549593 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24155240" @default.
• W2074549593 hasPublicationYear "2013" @default.
• W2074549593 type Work @default.
• W2074549593 sameAs 2074549593 @default.
• W2074549593 citedByCount "47" @default.
• W2074549593 countsByYear W20745495932013 @default.
• W2074549593 countsByYear W20745495932014 @default.
• W2074549593 countsByYear W20745495932015 @default.
• W2074549593 countsByYear W20745495932016 @default.
• W2074549593 countsByYear W20745495932017 @default.
• W2074549593 countsByYear W20745495932018 @default.
• W2074549593 countsByYear W20745495932019 @default.
• W2074549593 countsByYear W20745495932020 @default.
• W2074549593 countsByYear W20745495932021 @default.
• W2074549593 countsByYear W20745495932022 @default.
• W2074549593 countsByYear W20745495932023 @default.
• W2074549593 crossrefType "journal-article" @default.
• W2074549593 hasAuthorship W2074549593A5006128068 @default.
• W2074549593 hasAuthorship W2074549593A5012827429 @default.
• W2074549593 hasAuthorship W2074549593A5014787862 @default.
• W2074549593 hasAuthorship W2074549593A5018496662 @default.
• W2074549593 hasAuthorship W2074549593A5019361653 @default.
• W2074549593 hasAuthorship W2074549593A5050117572 @default.
• W2074549593 hasAuthorship W2074549593A5053111848 @default.
• W2074549593 hasAuthorship W2074549593A5060591351 @default.
• W2074549593 hasAuthorship W2074549593A5066477976 @default.
• W2074549593 hasAuthorship W2074549593A5076385970 @default.
• W2074549593 hasAuthorship W2074549593A5080561801 @default.

• next