ArticleJournal of lipid research2015
Metabolomics reveal 1-palmitoyl lysophosphatidylcholine production by peroxisome proliferator-activated receptor α.
Article in Journal of lipid research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Metabolic profiling of human follicular fluid to unravel the pathways involved in polycystic ovary syndrome - a systematic review.Reviews in endocrine & metabolic disorders · 2026Pooled it
- Endocrine regulation of the hepatic fasting response: cues, cooperation and consequences.Nature reviews. Endocrinology · 2026Review
- Gastrectomy promoted diabetes remission involves the molecular clock and epigenetic mechanisms in a rat model of lean type 2 diabetes.Scientific reports · 2025Article
- Abdominal obesity in youth: the associations of plasma Lysophophatidylcholine concentrations with insulin resistance.Pediatric research · 2025Article
- Repeated fasting events sensitize enhancers, transcription factor activity and gene expression to support augmented ketogenesis.Nucleic acids research · 2025Article
- Bezafibrate Reduces Elevated Hepatic Fumarate in Insulin-Deficient Mice.Biomedicines · 2022Article
- Article
- Chronic Effect of a Cafeteria Diet and Intensity of Resistance Training on the Circulating Lysophospholipidome in Young Rats.Metabolites · 2021Article
- Metabolome analysis revealed that soybean-Aspergillus oryzae interaction induced dynamic metabolic and daidzein prenylation changes.PloS one · 2021Article
- Lipidomics Reveals the Therapeutic Effects of EtOAc Extract ofFrontiers in pharmacology · 2020Article
- Lifestyle and Food Habits Impact on Chronic Diseases: Roles of PPARs.International journal of molecular sciences · 2019Review
- Article
- Metabolomic and lipidomic analysis of the effect of pioglitazone on hepatic steatosis in a rat model of obese Type 2 diabetes.British journal of pharmacology · 2018Article
- Transcriptional programming of lipid and amino acid metabolism by the skeletal muscle circadian clock.PLoS biology · 2018Article
- The Peroxisome Proliferator-Activated Receptor α (PPARα) Agonist Pemafibrate Protects against Diet-Induced Obesity in Mice.International journal of molecular sciences · 2018Article
- Wide-range screening of anti-inflammatory compounds in tomato using LC-MS and elucidating the mechanism of their functions.PloS one · 2018Article
- The hepatokine FGF21 is crucial for peroxisome proliferator-activated receptor-α agonist-induced amelioration of metabolic disorders in obese mice.The Journal of biological chemistry · 2017Article
- Graphene Oxide as a Novel Evenly Continuous Phase Matrix for TOF-SIMS.Journal of the American Society for Mass Spectrometry · 2017Article
- Muscle and liver-specific alterations in lipid and acylcarnitine metabolism after a single bout of exercise in mice.Scientific reports · 2016Article
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PPARα is well known as a master regulator of lipid metabolism. PPARα activation enhances fatty acid oxidation and decreases the levels of circulating and cellular lipids in obese diabetic patients. Although PPARα target genes are widely known, little is known about the alteration of plasma and liver metabolites during PPARα activation. Here, we report that metabolome analysis-implicated upregulation of many plasma lysoGP species during bezafibrate (PPARα 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 PPARα activation, and this effect was attenuated by PPARα antagonist treatment. We demonstrated that Pla2g7 gene expression levels in the murine hepatocytes were increased by PPARα activation, and the secretion of LPC(16:0) was suppressed by Pla2g7 siRNA treatment. Interestingly, LPC(16:0) activates PPARα and induces the expression of PPARα 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 PPARα activation in hepatocytes; LPC(16:0) contributes to the upregulation of PPARα target genes in hepatocytes and the recovery of glucose uptake in insulin-resistant adipocytes.
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