Diet impact on mitochondrial bioenergetics and dynamics

http://journal.frontiersin.org/article/10.3389/fphys.2015.00109/full

Rosalba Putti, Raffaella Sica, Vincenzo Migliaccio and Lillà Lionetti

 

In this study they investigate the effect of two different fat dietary sources (saturated (HL diet) vs polyunsaturated (HFO diet) omega 3 ) on mitochondrial dynamics and function in rat liver and skeletal muscle. The consequences of starvation and caloric restriction (CR) are also discussed.

The high fat diet rich in saturated fatty acid (HL diet) decreases mitochondrial function and increases ROS production. Mitochondria became more fragmented. Mitochondria do become more efficient due to a decrease in proton leak. An increase in energy efficiency reduces energy expenditure and can contribute to obesity development. In several studies it has been suggested that decreases in Mfn2 lead to decreases in proton leak. Mfn2 has also been linked to regulation of in vivo insulin resistance. Increased mitochondrial fragmentation induced by HL diet may be an adaptive cellular response to increase oxidation of surplus dietary fatty acids, which results in higher ROS production.

In contrast to the HL diet, the HFO diet rich in polyunsaturated fatty acids seems to improve mitochondrial function. ROS production is reduced, and increased mitochondrial fusion is seen. HFO diet also leads to a mild mitochondrial uncoupling due to enhanced expression of uncoupling protein 2. Mitochondrial efficiency is thus decreased, which may explain the decrease in ROS and observed increase in fatty acid utilization. There was less weight gain in rats with HFO diet compared to rats with HL diet.

Opposite effects on mitochondrial dynamics are seen for two types of nutrient deficiency, starvation and caloric restriction (CR):

Upon starvation, mitochondria fuse, has been associated with increases in ATP production. The fusion of mitochondria during starvation has been suggested to maximize energy production to sustain the cell during nutrient deprivation.

On the other hand, CR (e.g. mice submitted to 40% CR for 6 months) leads to mitochondrial fission. Mitochondrial biogenesis also increases. The larger number of mitochondria seen was linked to a reduction in oxygen consumption, membrane potential and ROS. Levels of ATP production were no different in CR conditions vs. control. It is like the cell increases the number of mitochondria so that each mitochondrion works less hard, which then decreases ROS. Having mitochondria fragmented also means that dysfunctional mitochondria can be more easily degraded.