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Genetic dissection of retinoid esterification and accumulation in the liver and adipose tissue

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Genetic dissection of retinoid esterification and accumulation in the liver and adipose tissue. / Wongsiriroj, Nuttaporn; Jiang, Hongfeng; Piantedosi, Roseann; Yang, Kryscilla Jian Zhang; Kluwe, Johannes; Schwabe, Robert F; Ginsberg, Henry; Goldberg, Ira J; Blaner, William S.

in: J LIPID RES, Jahrgang 55, Nr. 1, 01.01.2014, S. 104-114.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Wongsiriroj, N, Jiang, H, Piantedosi, R, Yang, KJZ, Kluwe, J, Schwabe, RF, Ginsberg, H, Goldberg, IJ & Blaner, WS 2014, 'Genetic dissection of retinoid esterification and accumulation in the liver and adipose tissue', J LIPID RES, Jg. 55, Nr. 1, S. 104-114. https://doi.org/10.1194/jlr.M043844

APA

Wongsiriroj, N., Jiang, H., Piantedosi, R., Yang, K. J. Z., Kluwe, J., Schwabe, R. F., Ginsberg, H., Goldberg, I. J., & Blaner, W. S. (2014). Genetic dissection of retinoid esterification and accumulation in the liver and adipose tissue. J LIPID RES, 55(1), 104-114. https://doi.org/10.1194/jlr.M043844

Vancouver

Wongsiriroj N, Jiang H, Piantedosi R, Yang KJZ, Kluwe J, Schwabe RF et al. Genetic dissection of retinoid esterification and accumulation in the liver and adipose tissue. J LIPID RES. 2014 Jan 1;55(1):104-114. https://doi.org/10.1194/jlr.M043844

Bibtex

@article{b2f8dcd3bfcd4070b3d4b46a65138aa4,
title = "Genetic dissection of retinoid esterification and accumulation in the liver and adipose tissue",
abstract = "Approximately 80-90% of all retinoids in the body are stored as retinyl esters (REs) in the liver. Adipose tissue also contributes significantly to RE storage. The present studies, employing genetic and nutritional interventions, explored factors that are responsible for regulating RE accumulation in the liver and adipose tissue and how these influence levels of retinoic acid (RA) and RA-responsive gene expression. Our data establish that acyl-CoA:retinol acyltransferase (ARAT) activity is not involved in RE synthesis in the liver, even when mice are nutritionally stressed by feeding a 25-fold excess retinol diet or upon ablation of cellular retinol-binding protein type I (CRBPI), which is proposed to limit retinol availability to ARATs. Unlike the liver, where lecithin:retinol acyltransferase (LRAT) is responsible for all RE synthesis, this is not true for adipose tissue where Lrat-deficient mice display significantly elevated RE concentrations. However, when CrbpI is also absent, RE levels resemble wild-type levels, suggesting a role for CrbpI in RE accumulation in adipose tissue. Although expression of several RA-responsive genes is elevated in Lrat-deficient liver, employing a sensitive liquid chromatography tandem mass spectrometry protocol and contrary to what has been assumed for many years, we did not detect elevated concentrations of all-trans-RA. The elevated RA-responsive gene expression was associated with elevated hepatic triglyceride levels and decreased expression of Pparδ and its downstream Pdk4 target, suggesting a role for RA in these processes in vivo.",
keywords = "Adipose Tissue, White, Animals, Epididymis, Esterification, Esters, Female, Gene Expression, Gene Expression Regulation, Liver, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, PPAR delta, Phosphatidylcholine-Sterol O-Acyltransferase, Protein-Serine-Threonine Kinases, Retinoids, Retinol O-Fatty-Acyltransferase, Retinol-Binding Proteins, Cellular, Triglycerides",
author = "Nuttaporn Wongsiriroj and Hongfeng Jiang and Roseann Piantedosi and Yang, {Kryscilla Jian Zhang} and Johannes Kluwe and Schwabe, {Robert F} and Henry Ginsberg and Goldberg, {Ira J} and Blaner, {William S}",
year = "2014",
month = jan,
day = "1",
doi = "10.1194/jlr.M043844",
language = "English",
volume = "55",
pages = "104--114",
journal = "J LIPID RES",
issn = "0022-2275",
publisher = "American Society for Biochemistry and Molecular Biology Inc.",
number = "1",

}

RIS

TY - JOUR

T1 - Genetic dissection of retinoid esterification and accumulation in the liver and adipose tissue

AU - Wongsiriroj, Nuttaporn

AU - Jiang, Hongfeng

AU - Piantedosi, Roseann

AU - Yang, Kryscilla Jian Zhang

AU - Kluwe, Johannes

AU - Schwabe, Robert F

AU - Ginsberg, Henry

AU - Goldberg, Ira J

AU - Blaner, William S

PY - 2014/1/1

Y1 - 2014/1/1

N2 - Approximately 80-90% of all retinoids in the body are stored as retinyl esters (REs) in the liver. Adipose tissue also contributes significantly to RE storage. The present studies, employing genetic and nutritional interventions, explored factors that are responsible for regulating RE accumulation in the liver and adipose tissue and how these influence levels of retinoic acid (RA) and RA-responsive gene expression. Our data establish that acyl-CoA:retinol acyltransferase (ARAT) activity is not involved in RE synthesis in the liver, even when mice are nutritionally stressed by feeding a 25-fold excess retinol diet or upon ablation of cellular retinol-binding protein type I (CRBPI), which is proposed to limit retinol availability to ARATs. Unlike the liver, where lecithin:retinol acyltransferase (LRAT) is responsible for all RE synthesis, this is not true for adipose tissue where Lrat-deficient mice display significantly elevated RE concentrations. However, when CrbpI is also absent, RE levels resemble wild-type levels, suggesting a role for CrbpI in RE accumulation in adipose tissue. Although expression of several RA-responsive genes is elevated in Lrat-deficient liver, employing a sensitive liquid chromatography tandem mass spectrometry protocol and contrary to what has been assumed for many years, we did not detect elevated concentrations of all-trans-RA. The elevated RA-responsive gene expression was associated with elevated hepatic triglyceride levels and decreased expression of Pparδ and its downstream Pdk4 target, suggesting a role for RA in these processes in vivo.

AB - Approximately 80-90% of all retinoids in the body are stored as retinyl esters (REs) in the liver. Adipose tissue also contributes significantly to RE storage. The present studies, employing genetic and nutritional interventions, explored factors that are responsible for regulating RE accumulation in the liver and adipose tissue and how these influence levels of retinoic acid (RA) and RA-responsive gene expression. Our data establish that acyl-CoA:retinol acyltransferase (ARAT) activity is not involved in RE synthesis in the liver, even when mice are nutritionally stressed by feeding a 25-fold excess retinol diet or upon ablation of cellular retinol-binding protein type I (CRBPI), which is proposed to limit retinol availability to ARATs. Unlike the liver, where lecithin:retinol acyltransferase (LRAT) is responsible for all RE synthesis, this is not true for adipose tissue where Lrat-deficient mice display significantly elevated RE concentrations. However, when CrbpI is also absent, RE levels resemble wild-type levels, suggesting a role for CrbpI in RE accumulation in adipose tissue. Although expression of several RA-responsive genes is elevated in Lrat-deficient liver, employing a sensitive liquid chromatography tandem mass spectrometry protocol and contrary to what has been assumed for many years, we did not detect elevated concentrations of all-trans-RA. The elevated RA-responsive gene expression was associated with elevated hepatic triglyceride levels and decreased expression of Pparδ and its downstream Pdk4 target, suggesting a role for RA in these processes in vivo.

KW - Adipose Tissue, White

KW - Animals

KW - Epididymis

KW - Esterification

KW - Esters

KW - Female

KW - Gene Expression

KW - Gene Expression Regulation

KW - Liver

KW - Male

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - PPAR delta

KW - Phosphatidylcholine-Sterol O-Acyltransferase

KW - Protein-Serine-Threonine Kinases

KW - Retinoids

KW - Retinol O-Fatty-Acyltransferase

KW - Retinol-Binding Proteins, Cellular

KW - Triglycerides

U2 - 10.1194/jlr.M043844

DO - 10.1194/jlr.M043844

M3 - SCORING: Journal article

C2 - 24186946

VL - 55

SP - 104

EP - 114

JO - J LIPID RES

JF - J LIPID RES

SN - 0022-2275

IS - 1

ER -