In March, Samantha Adamson, MD, PhD; Sangeeta Adak, PhD; Max C. Petersen, MD, PhD; Dustin Higgins, DO; Larry D. Spears, PhD; Rong Mei Zhang, MD; Andrea Cedeno, MD; Alexis McKee, MD, CDCES; Aswathi Kumar, MD; Sudhir M. Singh, MD; Fong-Fu Hsu, PhD; Janet B. McGill, MD, MA, FACP; and Clay F. Semenkovich, MD had their article titled “Decreased sarcoplasmic reticulum phospholipids in human skeletal muscle are associated with metabolic syndrome,” published by the Journal of Lipid Research.
More than 40% of adults are affected by metabolic syndrome, which can increase the risk of diabetes, cardiovascular disease and all-cause mortality. A significant contributor to the development of metabolic syndrome is muscle insulin resistance.
In the article, the authors reference how current studies in mice have linked skeletal muscle sarcoplasmic reticulum (SR) phospholipid composition to sarcoplasmic/endoplasmic reticulum Ca2+-ATPase activity and insulin sensitivity. To further understand the pathogenesis of metabolic syndrome, they question if specific phosphatidylcholine (PC) and phosphatidylethanolamine (PE) species in human SR could be altered by the presence of metabolic syndrome.
By comparing “SR phospholipid composition in skeletal muscle from sedentary subjects with metabolic syndrome and sedentary control subjects without metabolic syndrome,” the authors observed a decrease of SR phospholipid content in the skeletal muscle of patients with metabolic syndrome.
Furthermore, their findings were “consistent with the existence of a relationship between skeletal muscle SR PC content and insulin resistance in humans,” support “preclinical observations linking SR phospholipid content to muscle insulin sensitivity,” and provide “a rationale for additional mechanistic investigations to determine if SR phospholipids interact with the regulation of insulin-stimulated glucose disposal in skeletal muscle.”
Decreased sarcoplasmic reticulum phospholipids in human skeletal muscle are associated with metabolic syndrome. Adamson, Samantha E. et al. Journal of Lipid Research, Volume 65, Issue 3, 100519. https://www.jlr.org/article/S0022-2275(24)00024-5/fulltext