Phosphatidyl choline

This study aimed to investigate the variations in aldehyde and ketone (AKs) concentrations and associated inhalation risks in emissions from heated rapeseed oils with different levels of non-acylglycerols. Firstly, the effect of heating temperatures and refining levels of the oil on the concentration and inhalation risk of AKs in the oil fumes was explored. The results revealed that full refining of rapeseed oil increased AKs concentration and associated inhalation risk, especially at higher temperatures. Subsequently, six representative non-acylglycerol components were added to the refined oil to investigate their effects on AKs. Results showed that both oleic acid and phosphatidylcholine increased the AKs concentrations and associated inhalation risks, whereas canolol, γ-tocopherol and β-carotene reduced the formation of AKs in refined oil fumes. Finally, the formation mechanism of AKs in oil fumes was analyzed. This work was intended to provide theoretical foundations for safer cooking practices and moderate processing of rapeseed oil.

Intervertebral disc degeneration (IDD) is a prevalent musculoskeletal disorder with substantial socioeconomic impacts. Despite its high prevalence, the pathogenesis of IDD remains unclear, and effective pharmacological interventions are lacking. This study aimed to investigate metabolic alterations in IDD and explore potential therapeutic targets by analyzing lipotoxicity‐related mechanisms in nucleus pulposus (NP) cells.

Metabolomics and magnetic resonance spectroscopy were utilized to profile metabolic changes in NP tissues from advanced‐stage IDD. Transcriptomics and metabolomics integration were performed to identify key regulatory pathways. In vitro experiments using human NP cells exposed to palmitic acid were conducted to evaluate endoplasmic reticulum (ER) stress, mitochondrial dysfunction, lipid droplet accumulation, and senescence. Phosphatidylcholine supplementation was tested for its ability to mitigate lipotoxicity, with ER‐mitochondria interactions and mitochondrial oxidation capacity assessed as mechanistic endpoints.

Our findings revealed an abnormal lipotoxic condition in NP cells from advanced‐stage IDD. Furthermore, we identified abnormal accumulation of triglycerides and palmitic acid in NP cells from IDD. The palmitic acid accumulation resulted in endoplasmic reticulum stress, mitochondrial damage, lipid droplet accumulation, and senescence of NP cells. By integrating transcriptomics and metabolomics analyses, we discovered that phosphatidylcholine plays a role in regulating palmitic acid‐induced lipotoxicity. Notably, phosphatidylcholine level was found to be low in the endoplasmic reticulum and mitochondria of advanced‐stage NP cells. Phosphatidylcholine treatment alleviated palmitic acid‐induced lipid droplet accumulation and senescence of NP cells by modulating ER‐mitochondria contacts and mitochondrial oxidation capacity.

Phosphatidylcholine emerges as a potential therapeutic agent to counteract lipotoxic stress by modulating organelle interactions and mitochondrial function. These findings advance our understanding of IDD pathogenesis and provide a novel metabolic target for therapeutic development.