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

DOI: 10.1186/gb-2007-8-3-r38

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Abstract:

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.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.Despite the overt recognition of the taxing effects of obesity on both medical and social programs throughout the world, the estimated 300 million adults currently considered clinically obese in addition to the universal increase in childhood obesity indicates we are still succumbing to this global epidemic. Indeed, the poorly understood gene-environment interactions have revealed the complexity of this metabolic disease; however, with each passing year an increasing number of genetic candidates are discovered that help to further unravel the perturbed metabolism underlying the obese phenotype [1,2]. Recently, phospholipid scramblase (Plscr) 3 was identified as a genetic candidate capable of influencing adipose function and, ultimately, the obese phenotype. Mice deficient in PLSCR3 were found to accumulate lipid in abdominal fat pads and were characterized with insulin resistance, dyslipidemia, and glucose intolerance, classic tell-tale markers for metab

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