title: Nutrient availability links mitochondria, apoptosis, and obesity.
abstract: Mitochondria are the dominant source of the cellular energy requirements through oxidative phosphorylation, but they are also central players in apoptosis. Nutrient availability may have been the main evolutionary driving force behind these opposite mitochondrial functions: production of energy to sustain life and release of apoptotic proteins to trigger cell death. Here, we explore the link between nutrients, mitochondria and apoptosis with known and potential implications for age-related decline and metabolic syndromes.
authors.affiliation: Medical Research Council, Toxicology Unit/University of Leicester, LE1 1QH, Leicester UK.
authors.forename: Francesca
authors.initials: F
authors.lastname: Pintus
authors.forename: Giovanni
authors.initials: G
authors.lastname: Floris
authors.forename: Alessandro
authors.initials: A
authors.lastname: Rufini
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D001682:Biological Availability; D004734:Energy Metabolism / Q000502:physiology*; D005502:Food; D006801:Humans; D008928:Mitochondria / Q000502:physiology*; D009753:Nutritive Value; D009765:Obesity / Q000378:metabolism*