Mitochondria play crucial role in the energetic metabolism, thermogenesis, maintenance of calcium homeostasis and apoptosis. Cyclic changes in fusion and fission of mitochondria are required for properly functioning organelles, especially in tissues with high dependence on energy supply such as skeletal muscles, heart, or neurons. The key role of mitochondrial fusion is observed in embryonic development and maintaining unchanged mtDNA pool under conditions of oxidative stress. There is a large number of data indicating that mitochondrial networks often accompany the resistance to apoptotic stimuli. In contrast to fusion – the mitochondrial fission precedes apoptosis. According to the newest knowledge precise interactions between a few proteins are required for mitochondrial fusion and division. Among them Drp1, Mfn1, Mfn2 and Opa1 are considered the most important. Recent reports shed some light on the physiological importance of proteins participating in mitochondrial membrane dynamics in energy production, apoptosis and cellular signaling. In this presentation the author reports on the recent knowledge concerning structural changes of mitochondria with a particular interest to transmembrane GTPases and their role in cellular physiology. This is especially important since Mfn2 GTP-ase controls the bioenergetics of muscle cells. Insulin increases the activity of Mfn2 and accelerates myogenesis, whereas repression of Mfn2 reduces glucose oxidation, mitochondrial membrane potential and cell respiration. Apparently, the regulation of energy expenditure in muscles by Mfn2 might play decissive role in the origin of obesity and non insulin-dependent diabetes.

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