Lipin deactivation after acetaminophen overdose causes phosphatidic acid accumulation in liver and plasma in mice and humans and enhances liver regeneration

Andrew J. Lutkewitte; George G. Schweitzer; Stefanie Kennon-McGill; Melissa M. Clemens; Laura P. James; Hartmut Jaeschke; Brian N. Finck; Mitchell R. McGill

doi:10.1016/j.fct.2018.03.014

Lipin deactivation after acetaminophen overdose causes phosphatidic acid accumulation in liver and plasma in mice and humans and enhances liver regeneration

Andrew J. Lutkewitte
, George G. Schweitzer
, Stefanie Kennon-McGill
, Melissa M. Clemens
, Laura P. James
, Hartmut Jaeschke
, Brian N. Finck
, Mitchell R. McGill

Research output: Contribution to journal › Article › peer-review

Original language	English
Pages (from-to)	273-283
Number of pages	11
Journal	Food and Chemical Toxicology
Volume	115
DOIs	https://doi.org/10.1016/j.fct.2018.03.014
State	Published - May 2018

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10.1016/j.fct.2018.03.014

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Lutkewitte, A. J., Schweitzer, G. G., Kennon-McGill, S., Clemens, M. M., James, L. P., Jaeschke, H., Finck, B. N., & McGill, M. R. (2018). Lipin deactivation after acetaminophen overdose causes phosphatidic acid accumulation in liver and plasma in mice and humans and enhances liver regeneration. Food and Chemical Toxicology, 115, 273-283. https://doi.org/10.1016/j.fct.2018.03.014

@article{c91654177e1044e88b98cec0789092fb,

title = "Lipin deactivation after acetaminophen overdose causes phosphatidic acid accumulation in liver and plasma in mice and humans and enhances liver regeneration",

author = "Lutkewitte, \{Andrew J.\} and Schweitzer, \{George G.\} and Stefanie Kennon-McGill and Clemens, \{Melissa M.\} and James, \{Laura P.\} and Hartmut Jaeschke and Finck, \{Brian N.\} and McGill, \{Mitchell R.\}",

note = "Funding Information: This work was supported in part by start-up funds from the University of Arkansas for Medical Sciences (to MRM). Other sources of support included an intramural grant (to BNF and MRM) and core facility services from the Washington University Institute of Clinical and Translational Sciences , which is funded in part by grant UL1TR000448 from the National Center for Advancing Translational Sciences (NCATS) of the National Institutes of Health (NIH) , and NIH grants R01 DK078187 and R01 HL119225 (to BNF). Mass spectrometry was performed in the Metabolomics Facility at Washington University ( NIH P30 DK056341 ). Additional support came from NIH grant T32 DK0077653 (AJL). MRM would also like to thank Drs. Mitchell G. Scott, Ann M. Gronowski, Dennis J. Dietzen, and Sarah Riley at Washington University School of Medicine and St. Louis University for additional support, and for excellent training in laboratory medicine. The funding sources had no role in design or execution of experiments, nor in writing this manuscript. ",

year = "2018",

month = may,

doi = "10.1016/j.fct.2018.03.014",

language = "English",

volume = "115",

pages = "273--283",

journal = "Food and Chemical Toxicology",

issn = "0278-6915",

}

Lutkewitte, AJ, Schweitzer, GG, Kennon-McGill, S, Clemens, MM, James, LP, Jaeschke, H, Finck, BN & McGill, MR 2018, 'Lipin deactivation after acetaminophen overdose causes phosphatidic acid accumulation in liver and plasma in mice and humans and enhances liver regeneration', Food and Chemical Toxicology, vol. 115, pp. 273-283. https://doi.org/10.1016/j.fct.2018.03.014

TY - JOUR

T1 - Lipin deactivation after acetaminophen overdose causes phosphatidic acid accumulation in liver and plasma in mice and humans and enhances liver regeneration

AU - Lutkewitte, Andrew J.

AU - Schweitzer, George G.

AU - Kennon-McGill, Stefanie

AU - Clemens, Melissa M.

AU - James, Laura P.

AU - Jaeschke, Hartmut

AU - Finck, Brian N.

AU - McGill, Mitchell R.

N1 - Funding Information: This work was supported in part by start-up funds from the University of Arkansas for Medical Sciences (to MRM). Other sources of support included an intramural grant (to BNF and MRM) and core facility services from the Washington University Institute of Clinical and Translational Sciences , which is funded in part by grant UL1TR000448 from the National Center for Advancing Translational Sciences (NCATS) of the National Institutes of Health (NIH) , and NIH grants R01 DK078187 and R01 HL119225 (to BNF). Mass spectrometry was performed in the Metabolomics Facility at Washington University ( NIH P30 DK056341 ). Additional support came from NIH grant T32 DK0077653 (AJL). MRM would also like to thank Drs. Mitchell G. Scott, Ann M. Gronowski, Dennis J. Dietzen, and Sarah Riley at Washington University School of Medicine and St. Louis University for additional support, and for excellent training in laboratory medicine. The funding sources had no role in design or execution of experiments, nor in writing this manuscript.

PY - 2018/5

Y1 - 2018/5

UR - https://www.scopus.com/pages/publications/85044169616

U2 - 10.1016/j.fct.2018.03.014

DO - 10.1016/j.fct.2018.03.014

M3 - Article

C2 - 29534981

AN - SCOPUS:85044169616

SN - 0278-6915

VL - 115

SP - 273

EP - 283

JO - Food and Chemical Toxicology

JF - Food and Chemical Toxicology

ER -

Lipin deactivation after acetaminophen overdose causes phosphatidic acid accumulation in liver and plasma in mice and humans and enhances liver regeneration

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