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Introduction Food intake is highly regulated and remains relatively stable during steady-state conditions (Cummings & Overduin, 2007), whilst highly plastic regulatory mechanisms allow food intake to adapt rapidly to changing metabolic demands. The gastrointestinal tract (GIT) plays a key role in the regulation of food intake by sensing food intake and signalling via vagal afferents to the CNS to modulate satiety (Cummings & Overduin, 2007).
Mitochondrial metabolism is a major determinant of insulin secretion from pancreatic ?-cells. Type 2 diabetes evolves when ?-cells fail to release appropriate amounts of insulin in response to glucose. This results in hyperglycemia and metabolic dysregulation. Evidence has recently been mounting that mitochondrial dysfunction plays an important role in these processes. Monogenic dysfunction of mitochondria is a rare condition but causes a type 2 diabetes-like syndrome owing to ?-cell failure.
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