Abstract
Fasting stimulates catabolic reactions in skeletal muscle to survive nutrient deprivation. Cellular phospholipids have large structural diversity due to various polar-heads and acyl-chains that affect many cellular functions. Skeletal muscle phospholipid profiles have been suggested to be associated with muscle adaptations to nutritional and environmental status. However, the effect of fasting on skeletal muscle phospholipid profiles remains unknown. Here, we analyzed phospholipids using liquid chromatography mass spectrometry. We determined that fasting resulted in a decrease in 22:6-containing phosphatidylcholines (PCs) (22:6-PCs) and an increase in 18:2-containing PCs (18:2-PCs). The fasting-induced increase in 18:2-PCs was sufficient to complement 22:6-PCs loss, resulting in the maintenance of the total amount of polyunsaturated fatty acid (PUFA)-containing PCs. Similar phospholipid alterations occurred in insulin-deficient mice, which indicate that these observed phospholipid perturbations were characteristic of catabolic skeletal muscle. In lysophosphatidic acid acyltransferase 3-knockout muscles that mostly lack 22:6-PCs, other PUFA-containing PCs, mainly 18:2-PCs, accumulated. This suggests a compensatory mechanism for skeletal muscles to maintain PUFA-containing PCs.
Highlights
Skeletal muscle adapts its metabolism to suit nutritional status and environmental conditions
As shown in the principal component analysis (PCA) score plots (Fig 1A), the second principal component (y-axis) scores of extensor digitorum longus (EDL) and soleus were clearly separated along the y-axis between the fed group and fast group, which indicates that prolonged fasting had a considerable effect on phospholipid profiles
Fasting increased certain 22:6-PCs, for example, PC (18:1/22:6) and PC (18:2/22:6) in the EDL, the decrease in PC (16:0/ 22:6) had a larger effect on the 22:6-PCs proportion that counteracted these minor effects (S1A and S1B Fig). These results suggest that the 22:6-PCs decreases during fasting are compensated by 18:2-PCs increases, which might play a role in maintaining polyunsaturated fatty acid (PUFA)-containing PCs at a consistent level in skeletal muscle
Summary
Skeletal muscle adapts its metabolism to suit nutritional status and environmental conditions. To investigate skeletal muscle phospholipid profiles, fatty acids derived from the phospholipid fraction extracted via thin-layer chromatography (TLC) or solid-phase separation were analyzed. Recent studies using liquid-chromatography mass spectrometry (MS) (LC-MS) and imaging MS, have enabled more accurate detection of each phospholipid species They provide a profound insight into skeletal muscle phospholipid alterations under several conditions, including exercise training [22, 23], muscle-wasting phenotype [24], and fiber-type specificity [25]. In lysophosphatidic acid acyltransferase (LPAAT) 3-KO muscles that mostly lack 22:6-PCs, other PUFA-containing PCs, especially 18:2-PCs, accumulate These results altogether suggest a compensatory mechanism by which skeletal muscle maintains the PUFA-containing PCs balance
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