Mobilization of pro-inflammatory lipids in obese Plscr3-deficient mice.

Mobilization of pro-inflammatory lipids in obese Plscr3-deficient mice. Research Abstract Details 

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Mobilization of pro-inflammatory lipids in obese Plscr3-deficient mice. Abstract Text:

David M Mutch,Grace O'Maille,William R Wikoff,Therese Wiedmer,Peter J Sims,Gary Siuzdak,

BACKGROUND: The obesity epidemic has prompted the search for candidate genes capable of influencing adipose function. One such candidate, that encoding phospholipid scramblase 3 (PLSCR3), was recently identified, as genetic deletion of it led to lipid accumulation in abdominal fat pads and changes characteristic of metabolic syndrome. Because adipose tissue is increasingly recognized as an endocrine organ, capable of releasing small molecules that modulate disparate physiological processes, we examined the plasma from wild-type, Plscr1-/-, Plscr3-/- and Plscr1&3-/- mice. Using an untargeted comprehensive metabolite profiling approach coupled with targeted gene expression analyses, the perturbed biochemistry and functional redundancy of PLSCR proteins was assessed. RESULTS: Nineteen metabolites were differentially and similarly regulated in both Plscr3-/- and Plscr1&3-/- animals, of which five were characterized from accurate mass, tandem mass spectrometry data and their correlation to the Metlin database as lysophosphatidylcholine (LPC) species enriched with C16:1, C18:1, C20:3, C20:5 and C22:5 fatty acids. No significant changes in the plasma metabolome were detected upon elimination of PLSCR1, indicating that increases in pro-inflammatory lipids are specifically associated with the obese state of Plscr3-deficient animals. Correspondingly, increases in white adipose lipogenic gene expression confirm a role for PLSCR3 in adipose lipid metabolism. CONCLUSION: The untargeted profiling of circulating metabolites suggests no detectable functional redundancies between PLSCR proteins; however, this approach simultaneously identified previously unrecognized lipid metabolites that suggest a novel molecular link between obesity, inflammation and the downstream consequences associated with PLSCR3-deficiency.

Mobilization of pro-inflammatory lipids in obese Plscr3-deficient mice. Publishing Authors By Initials

DM Mutch,G O'Maille,WR Wikoff,T Wiedmer,PJ Sims,G Siuzdak,

For similar investigative techniques: chemistry, analytical: mass spectrometry: tandem mass spectrometry research abstracts see: investigative techniques: chemistry, analytical: mass spectrometry: tandem mass spectrometry research

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Mobilization of pro-inflammatory lipids in obese Plscr3-deficient mice. Journal Published:

PUBLICATION TYPE: Research Support, U.S. Gov't,

Journal: Genome biology

VOLUME: 8

Page Numbers: R38

Journal Abbreviation: Genome Biol.

ISSN: 1465-6914

DAY: 3

MONTH: 12

YEAR: 2007

Mobilization of pro-inflammatory lipids in obese Plscr3-deficient mice. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100960660

Mobilization of pro-inflammatory lipids in obese Plscr3-deficient mice. Keywords Mesh Terms:

KEYWORDS: Tandem Mass Spectrometry

MESH TERMS: physiology

Chemical & Substance for Abstract: Mobilization of pro-inflammatory lipids in obese Plscr3-deficient mice. Information

Substance Name: Plscr3 protein, mouse

Registry Number: 0

Grant and Affiliation Information for Mobilization of pro-inflammatory lipids in obese Plscr3-deficient mice.

AFFILIATION: The Scripps Research Institute, Department of Molecular and Experimental Medicine, La Jolla, CA 92037, USA. dmmutch_sci@hotmail.com

Country: England

AGENCY: United States NIMH

GRANT: P30 MH062261

ACRONYM: MH

MEDLINETA: Genome Biol

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