Research Article: Nutrient availability links mitochondria, apoptosis, and obesity

Date Published: November 30, 2012

Publisher: Impact Journals LLC

Author(s): Francesca Pintus, Giovanni Floris, Alessandro Rufini.

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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.

Partial Text

The endosymbiotic theory proposes that mitochondria evolved from an atypical encounter of two prokaryotes that ended up in a symbiotic relationship. One bacterium was phagocytosed but not killed, and became progressively specialized in producing energy through oxidative phosphorylation – it became a mitochondrion. This pivotal event shaped the course of evolution, and was fundamental to the development of eukaryotic cells and metazoa [1, 2]. Progressively mitochondria turned into plastic organelles, specialized in energy production, but they also developed into an efficient cell-killing machine at the core of the apoptotic process. Growing evidence suggests that this mitochondrial apoptotic function is tightly linked to nutrient availability and respiratory efficiency, with important implications for health and aging.

 

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