| First Author | Gamu D | Year | 2019 |
| Journal | Am J Physiol Endocrinol Metab | Volume | 316 |
| Issue | 3 | Pages | E432-E442 |
| PubMed ID | 30601702 | Mgi Jnum | J:274295 |
| Mgi Id | MGI:6283116 | Doi | 10.1152/ajpendo.00288.2018 |
| Citation | Gamu D, et al. (2019) Phospholamban deficiency does not alter skeletal muscle SERCA pumping efficiency or predispose mice to diet-induced obesity. Am J Physiol Endocrinol Metab 316(3):E432-E442 |
| abstractText | The sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA) pump is a major contributor to skeletal muscle Ca(2+) homeostasis and metabolic rate. SERCA activity can become adaptively uncoupled by its regulator sarcolipin (SLN) to increase the energy demand of Ca(2+) pumping, preventing excessive obesity and glucose intolerance in mice. Several other SERCA regulators bear structural and functional resemblance to SLN, including phospholamban (PLN). Here, we sought to examine whether endogenous levels of skeletal muscle PLN control SERCA Ca(2+) pumping efficiency and whole body metabolism. Using PLN-null mice ( Pln(-/-)), we found that soleus (SOL) muscle's SERCA pumping efficiency (measured as an apparent coupling ratio: Ca(2+) uptake/ATP hydrolysis) was unaffected by PLN. Expression of Ca(2+)-handling proteins within the SOL, including SLN, were comparable between Pln(-/-) and wild-type (WT) littermates, as were fiber-type characteristics. Not surprisingly then, Pln(-/-) mice developed a similar degree of diet-induced obesity and glucose intolerance as WT controls when given a "Western" high-fat diet. Lack of an excessively obesogenic phenotype of Pln(-/-) could not be explained by compensation from skeletal muscle SLN or brown adipose tissue uncoupling protein-1 content. In agreement with several other reports, our study lends support to the notion that PLN serves a functionally distinct role from that of SLN in skeletal muscle physiology. |
