Inactivation of the mitochondrial carrier SLC25A25 (ATP-Mg2+/Pi transporter) reduces physical endurance and metabolic efficiency in mice.

摘要: An ATP-Mg2+/Pi inner mitochondrial membrane solute transporter (SLC25A25), which is induced during adaptation to cold stress in the skeletal muscle of mice with defective UCP1/brown adipose tissue thermogenesis, has been evaluated for its role metabolic efficiency. SLC25A25 thought control ATP homeostasis by functioning as a Ca2+-regulated shuttle ATP-Mg2+ and Pi across membrane. Mice an inactivated Slc25a25 gene have reduced efficiency evidenced enhanced resistance diet-induced obesity impaired exercise performance on treadmill. Mouse embryo fibroblasts from Slc25a25−/− Ca2+ flux endoplasmic reticulum, basal respiration, content. Although are metabolically inefficient, source inefficiency not primary function because maintain body temperature upon acute exposure (4 °C). Rather, most likely linked physical endurance test mutant Consequently, absence production required diminished secondary effects adiposity. However, UCP1-based induction intact may contribute alternative thermogenic pathway maintenance stress.