| First Author | Verkerke ARP | Year | 2019 |
| Journal | Nat Metab | Volume | 1 |
| Issue | 9 | Pages | 876-885 |
| PubMed ID | 32405618 | Mgi Jnum | J:299421 |
| Mgi Id | MGI:6500773 | Doi | 10.1038/s42255-019-0111-2 |
| Citation | Verkerke ARP, et al. (2019) Phospholipid methylation regulates muscle metabolic rate through Ca(2+) transport efficiency. Nat Metab 1(9):876-885 |
| abstractText | The biophysical environment of membrane phospholipids affects structure, function, and stability of membrane-bound proteins.(1,2) Obesity can disrupt membrane lipids, and in particular, alter the activity of sarco/endoplasmic reticulum (ER/SR) Ca(2+)-ATPase (SERCA) to affect cellular metabolism.(3-5) Recent evidence suggests that transport efficiency (Ca(2+) uptake / ATP hydrolysis) of skeletal muscle SERCA can be uncoupled to increase energy expenditure and protect mice from diet-induced obesity.(6,7) In isolated SR vesicles, membrane phospholipid composition is known to modulate SERCA efficiency.(8-11) Here we show that skeletal muscle SR phospholipids can be altered to decrease SERCA efficiency and increase whole-body metabolic rate. The absence of skeletal muscle phosphatidylethanolamine (PE) methyltransferase (PEMT) promotes an increase in skeletal muscle and whole-body metabolic rate to protect mice from diet-induced obesity. The elevation in metabolic rate is caused by a decrease in SERCA Ca(2+)-transport efficiency, whereas mitochondrial uncoupling is unaffected. Our findings support the hypothesis that skeletal muscle energy efficiency can be reduced to promote protection from obesity. |
