| First Author | Takahashi H | Year | 2015 |
| Journal | J Lipid Res | Volume | 56 |
| Issue | 2 | Pages | 254-65 |
| PubMed ID | 25510248 | Mgi Jnum | J:219829 |
| Mgi Id | MGI:5629797 | Doi | 10.1194/jlr.M052464 |
| Citation | Takahashi H, et al. (2015) Metabolomics reveal 1-palmitoyl lysophosphatidylcholine production by peroxisome proliferator-activated receptor alpha. J Lipid Res 56(2):254-65 |
| abstractText | PPARalpha is well known as a master regulator of lipid metabolism. PPARalpha activation enhances fatty acid oxidation and decreases the levels of circulating and cellular lipids in obese diabetic patients. Although PPARalpha target genes are widely known, little is known about the alteration of plasma and liver metabolites during PPARalpha activation. Here, we report that metabolome analysis-implicated upregulation of many plasma lysoGP species during bezafibrate (PPARalpha agonist) treatment. In particular, 1-palmitoyl lysophosphatidylcholine [LPC(16:0)] is increased by bezafibrate treatment in both plasma and liver. In mouse primary hepatocytes, the secretion of LPC(16:0) increased on PPARalpha activation, and this effect was attenuated by PPARalpha antagonist treatment. We demonstrated that Pla2g7 gene expression levels in the murine hepatocytes were increased by PPARalpha activation, and the secretion of LPC(16:0) was suppressed by Pla2g7 siRNA treatment. Interestingly, LPC(16:0) activates PPARalpha and induces the expression of PPARalpha target genes in hepatocytes. Furthermore, we showed that LPC(16:0) has the ability to recover glucose uptake in adipocytes induced insulin resistance. These results reveal that LPC(16:0) is induced by PPARalpha activation in hepatocytes; LPC(16:0) contributes to the upregulation of PPARalpha target genes in hepatocytes and the recovery of glucose uptake in insulin-resistant adipocytes. |
