Review Volume 4, Issue 11 pp 734—741

Nutrient availability links mitochondria, apoptosis, and obesity


Figure 2. Mitochondrial apoptosis links nutritional status with metabolic syndromes. Caloric restriction leads to an improvement of the mitochondrial function stimulating mitochondrial biogenesis and fusion, and increasing ETC efficiency with a decreased production of ROS. High caloric intake decreases levels of PCG-1α and Mfn2 leading to reduced mitochondrial fusion and compromising organelle functions. Moreover, in obesity apoptotic pathways proteins are upregulated and increased apoptosis has been reported in adipocytes. This cell death is strongly dependent on mitochondria as the extrinsic pathway can also activate the intrinsic pathway by caspase-8 mediated cleavage of the BH3-only protein Bid, resulting in the formation of the active truncated isoform tBid. Genetic depletion of Bid protects against obesity-induced metabolic syndrome. Other cell lines, such stem cells, might suffer a similar mitochondrial dysfunction during obesity and become more sensitive to apoptosis, which in turn, will worsen age and age-related metabolic syndromes.