Role of creatine and creatine kinase in UCP1-independent adipocyte thermogenesis.
Here, it is tended to argue for an alternative mechanism based on the classical CK/phosphocreatine shuttle and phosphocreatingine-driven futile Ca2+-cycling at the endoplasmic reticulum.
Abstract
During recent years, creatine kinase (CK) and its substrates phosphocreatine and creatine emerged as important players in uncoupling protein 1-independent, ATP-dependent non-shivering thermogenesis in beige/brown adipocytes. The exact thermogenic mechanism, that is facilitated by the CK system, however, still remains elusive. A futile creatine-cycling mechanism functioning via a hypothetical phosphocreatine phosphatase has been proposed. However, the molecular basis of such cycling remained elusive, so far. Here, we tend to argue for an alternative mechanism based on the classical CK/phosphocreatine shuttle and phosphocreatine-driven futile Ca2+-cycling at the endoplasmic reticulum.