| First Author | Mason RR | Year | 2014 |
| Journal | Mol Metab | Volume | 3 |
| Issue | 6 | Pages | 652-63 |
| PubMed ID | 25161888 | Mgi Jnum | J:221539 |
| Mgi Id | MGI:5640930 | Doi | 10.1016/j.molmet.2014.06.002 |
| Citation | Mason RR, et al. (2014) PLIN5 deletion remodels intracellular lipid composition and causes insulin resistance in muscle. Mol Metab 3(6):652-63 |
| abstractText | Defective control of lipid metabolism leading to lipotoxicity causes insulin resistance in skeletal muscle, a major factor leading to diabetes. Here, we demonstrate that perilipin (PLIN) 5 is required to couple intramyocellular triacylglycerol lipolysis with the metabolic demand for fatty acids. PLIN5 ablation depleted triacylglycerol stores but increased sphingolipids including ceramide, hydroxylceramides and sphingomyelin. We generated perilipin 5 (Plin5)(-/-) mice to determine the functional significance of PLIN5 in metabolic control and insulin action. Loss of PLIN5 had no effect on body weight, feeding or adiposity but increased whole-body carbohydrate oxidation. Plin5 (-/-) mice developed skeletal muscle insulin resistance, which was associated with ceramide accumulation. Liver insulin sensitivity was improved in Plin5 (-/-) mice, indicating tissue-specific effects of PLIN5 on insulin action. We conclude that PLIN5 plays a critical role in coordinating skeletal muscle triacylglycerol metabolism, which impacts sphingolipid metabolism, and is requisite for the maintenance of skeletal muscle insulin action. |
