Abstract
Phosphatidylcholine (PC) and phosphatidylethanolamine (PE), which make up the bulk of mammalian cell membrane phospholipids, are recognized for their importance in metabolic health. Perturbations in the ratio of PC:PE can affect membrane integrity and function, which thus have serious health consequences. Imbalance in the hepatic PC and PE membrane content can be linked to metabolic disturbances such as ER stress, fatty liver and insulin resistance. Given that impaired insulin sensitivity underlies the pathology of many metabolic disorders and skeletal muscle is a significant regulator of energy metabolism, it is likely that aberrant phospholipid metabolism in skeletal muscle affects whole-body insulin sensitivity. Sarco/endoplasmic reticulum Ca 2+ ATPase (SERCA) activity and mitochondrial function respond to alterations in PC:PE ratio and are associated with glucose homeostasis. Moreover, PC and PE content within the mitochondrial membrane influence mitochondrial respiration and biogenesis and thus, metabolic function. As skeletal muscle phospholipids respond to stimuli such as diet and exercise, understanding the implications of imbalances in PC:PE ratio is of great importance in the face of the rising epidemic of obesity related diseases. This review will summarize the current state of knowledge signifying the links between skeletal muscle PC:PE ratio and insulin sensitivity with respects to PC and PE metabolism, SERCA activity, mitochondrial function and exercise.
Highlights
Phosphatidylcholine (PC) and phosphatidylethanolamine (PE) are the most abundant phospholipids in mammalian cell membranes, with PC accounting for 45%–50% and PE for 15%–25% of the total lipid content[1]
Whether skeletal muscle PC:PE ratio plays a direct role in insulin sensitively is unclear; these findings suggest possible associations between PC and PE content and insulin resistance that warrant further investigation
Given that reduced muscle mitochondrial function is associated with insulin resistance in skeletal muscle[64–65,91], it is likely that imbalances in the mitochondrial PC:PE ratio can play a modulatory role in muscular insulin sensitivity
Summary
Phosphatidylcholine (PC) and phosphatidylethanolamine (PE) are the most abundant phospholipids in mammalian cell membranes, with PC accounting for 45%–50% and PE for 15%–25% of the total lipid content[1]. This finding is corroborated in choline/ethanolamine phosphotransferase 1 (CEPT1) knockdown in C2C12 myoblasts and muscle-specific knockout mice fed a high-fat diet where CEPT1 deficiency increases the SR PC:PE ratio and decreases SERCA activity to preserve insulin sensitivity[14]. Given that mitochondrial phospholipids influence mitochondrial biogenesis[63–64], bilayer-protein interactions[61], the activity of the electron transport system and mitochondrial function[62,65], skeletal muscle mitochondrial PC:PE ratio may be an important determinant of whole-body insulin sensitivity.
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