Effects of exertional dyspnea on early mobilization of patients with acute decompensated heart failure.

[Purpose] In this study, we investigated the association between exertional dyspnea and length of the mobilization program in patients with acute decompensated heart failure. [Participants and Methods] We recruited all consecutive patients with heart failure who were hemodynamically stabilized after administration of intravenous medication and were able to walk >10 m before admission. Exertional dyspnea was evaluated using the visual analog scale in all patients after the 10-m walk during each session of the mobilization program. Multiple regression analysis was used to determine the factors associated with length of the mobilization program. [Results] Our study included 52 patients. Multiple regression analysis showed that the length of the mobilization program was significantly associated with the visual analog scale on day 3 and the length before the start of the mobilization program; however, the length of the mobilization program showed no significant association with age and blood urea nitrogen levels. The standardized coefficients for the visual analog scale scores on day 3 and the length before the start of the mobilization program were 0.49 and 0.33, respectively. [Conclusion] Exertional dyspnea is a good predictor of the length of the mobilization program. Our findings highlight the importance of evaluation of exertional dyspnea.

Metabolomics reveal 1-palmitoyl lysophosphatidylcholine production by peroxisome proliferator-activated receptor α.

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.

Long-chain free fatty acid profiling analysis by liquid chromatography-mass spectrometry in mouse treated with peroxisome proliferator-activated receptor α agonist.

A change in the free fatty acid (FFA) profile reflects an alteration in the lipid metabolism of peripheral tissue. A high-throughput quantitative analysis method for individual FFAs therefore needs to be established. We report here an optimized LC-MS assay for a high-throughput and high-sensitivity analysis of the 10 major long-chain FFAs in mouse plasma and liver. This assay enables quantification of individual FFAs by using trace amounts of samples (2 µL of plasma and 10 mg of liver tissue). We apply this method to analyze the FFA profile of plasma and liver samples from an obese mouse model treated with bezafibrate, the peroxisome proliferator-activated receptor α (PPARα) agonist, and show a change in the FFA profile, particularly in the palmitoleic and oleic acid contents. This assay is useful for quantifying individual FFAs and helpful for monitoring the condition of lipid metabolism.