Dynamic process of lipid deterioration in hickory: Mechanism analysis of metabolic imbalance, membrane damage and repair dysfunction based on multi-omics.

Hickory nuts were nutrient-rich but were prone to storage deterioration due to high fat content. In this study, using integrated lipidomics and transcriptomics, we profiled 2159 lipids and 5952 differentially expressed genes in hickories stored at 4 °C and 35 °C for 90 days. Results showed that oxidative stress decreased iodine value and increased anisidine and conjugated diene values, reflecting reduced lipid unsaturation and oxidation product accumulation. Upregulation of TGL4 and PLD1_2 accelerated triglyceride and phospholipid hydrolysis. However, ACAA1 downregulation inhibited free fatty acid catabolism generated during this process, which promoted off-flavor generation and anomalous triglyceride accumulation via re-esterification. Additionally, downregulation of DGKs and FAB2 caused the gradual accumulation of LPCs and Cer, disrupting sphingolipid balance and membrane integrity. This multi-omics study elucidates how dysregulation of lipid repair and sphingolipid disruption lead to accelerated oxidation during hickory storage. The findings supported Sustainable Development Goal 12.3 by informing strategies to reduce postharvest nut losses.