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• W2254934739 endingPage "7003" @default.
• W2254934739 startingPage "6989" @default.
• W2254934739 abstract "Ceramides are bioactive sphingolipids, which are composed of sphingoid bases carrying acyl chains of various lengths. Ceramides are synthesized by a family of six ceramide synthases (CerS) in mammals, which produce ceramides with different N-linked acyl chains. Increased ceramide levels are known to contribute to the development of obesity and insulin resistance. Recently, it has been demonstrated that the ceramide acylation pattern is of particular importance for an organism to maintain energy homeostasis. However, which of the CerS family members are involved in this process is not yet completely known. Using newly developed CerS5 knock-out mice, we show here that CerS5 is essential to maintain cellular C16:0 sphingolipid pools in lung, spleen, muscle, liver, and white adipose tissue. Glycerophospholipid levels in CerS5-deficient mice were not altered. We found a strong impact of CerS5-dependent ceramide synthesis in white adipose tissue after high fat diet feeding. In skeletal muscle, liver, and spleen, C16:0-ceramide levels were altered independent of feeding conditions. The loss of CerS5 is associated with reduced weight gain and improved systemic health, including maintenance of glucose homeostasis and reduced white adipose tissue inflammation after high fat diet challenge. Our findings indicate that reduction of endogenous C16:0-ceramide by genetic inhibition of CerS5 is sufficient to ameliorate obesity and its comorbidities. Ceramides are bioactive sphingolipids, which are composed of sphingoid bases carrying acyl chains of various lengths. Ceramides are synthesized by a family of six ceramide synthases (CerS) in mammals, which produce ceramides with different N-linked acyl chains. Increased ceramide levels are known to contribute to the development of obesity and insulin resistance. Recently, it has been demonstrated that the ceramide acylation pattern is of particular importance for an organism to maintain energy homeostasis. However, which of the CerS family members are involved in this process is not yet completely known. Using newly developed CerS5 knock-out mice, we show here that CerS5 is essential to maintain cellular C16:0 sphingolipid pools in lung, spleen, muscle, liver, and white adipose tissue. Glycerophospholipid levels in CerS5-deficient mice were not altered. We found a strong impact of CerS5-dependent ceramide synthesis in white adipose tissue after high fat diet feeding. In skeletal muscle, liver, and spleen, C16:0-ceramide levels were altered independent of feeding conditions. The loss of CerS5 is associated with reduced weight gain and improved systemic health, including maintenance of glucose homeostasis and reduced white adipose tissue inflammation after high fat diet challenge. Our findings indicate that reduction of endogenous C16:0-ceramide by genetic inhibition of CerS5 is sufficient to ameliorate obesity and its comorbidities." @default.
• W2254934739 created "2016-06-24" @default.
• W2254934739 creator A5002543787 @default.
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• W2254934739 date "2016-03-01" @default.
• W2254934739 modified "2023-10-15" @default.
• W2254934739 title "Ceramide Synthase 5 Is Essential to Maintain C16:0-Ceramide Pools and Contributes to the Development of Diet-induced Obesity" @default.
• W2254934739 cites W1872366297 @default.
• W2254934739 cites W1930548203 @default.
• W2254934739 cites W1951724000 @default.
• W2254934739 cites W1966595105 @default.
• W2254934739 cites W1969734540 @default.
• W2254934739 cites W1978051650 @default.
• W2254934739 cites W1978680304 @default.
• W2254934739 cites W1978918501 @default.
• W2254934739 cites W1981224101 @default.
• W2254934739 cites W1981231989 @default.
• W2254934739 cites W1982703175 @default.
• W2254934739 cites W1984413737 @default.
• W2254934739 cites W1992303307 @default.
• W2254934739 cites W1994472770 @default.
• W2254934739 cites W1995126002 @default.
• W2254934739 cites W1995392322 @default.
• W2254934739 cites W1995687483 @default.
• W2254934739 cites W2005658789 @default.
• W2254934739 cites W2013222950 @default.
• W2254934739 cites W2013392094 @default.
• W2254934739 cites W2014671368 @default.
• W2254934739 cites W2014728485 @default.
• W2254934739 cites W2015963944 @default.
• W2254934739 cites W2017859854 @default.
• W2254934739 cites W2018474075 @default.
• W2254934739 cites W2021032365 @default.
• W2254934739 cites W2024354971 @default.
• W2254934739 cites W2028320377 @default.
• W2254934739 cites W2032919119 @default.
• W2254934739 cites W2032919742 @default.
• W2254934739 cites W2034385545 @default.
• W2254934739 cites W2040280675 @default.
• W2254934739 cites W2041254182 @default.
• W2254934739 cites W2050704037 @default.
• W2254934739 cites W2051303794 @default.
• W2254934739 cites W2051970831 @default.
• W2254934739 cites W2066704041 @default.
• W2254934739 cites W2073115843 @default.
• W2254934739 cites W2073656642 @default.
• W2254934739 cites W2079608062 @default.
• W2254934739 cites W2090241387 @default.
• W2254934739 cites W2090475270 @default.
• W2254934739 cites W2093594635 @default.
• W2254934739 cites W2093816724 @default.
• W2254934739 cites W2101441343 @default.
• W2254934739 cites W2101951807 @default.
• W2254934739 cites W2109270957 @default.
• W2254934739 cites W2112583319 @default.
• W2254934739 cites W2124473191 @default.
• W2254934739 cites W2126188293 @default.
• W2254934739 cites W2133966719 @default.
• W2254934739 cites W2135160600 @default.
• W2254934739 cites W2135346216 @default.
• W2254934739 cites W2135354472 @default.
• W2254934739 cites W2145325288 @default.
• W2254934739 cites W2147382256 @default.
• W2254934739 cites W2150013759 @default.
• W2254934739 cites W2150437727 @default.
• W2254934739 cites W2150702412 @default.
• W2254934739 cites W2154070747 @default.
• W2254934739 cites W2156280702 @default.
• W2254934739 cites W2159267296 @default.
• W2254934739 cites W2162940414 @default.
• W2254934739 cites W2165711524 @default.
• W2254934739 cites W2167485774 @default.
• W2254934739 cites W2172149806 @default.
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• W2254934739 doi "https://doi.org/10.1074/jbc.m115.691212" @default.
• W2254934739 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4807283" @default.
• W2254934739 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26853464" @default.
• W2254934739 hasPublicationYear "2016" @default.
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