The anorectic anx/anx mouse, characterized by reduced food intake, is an interesting and useful model for studies of mechanisms involved in the regulation of food intake and anorexia. The anorexia (anx ) mutation arose spontaneously at the Jackson laboratory in 1976 and has now been mapped to a 0.2 cM interval on chromosome 2 (Chr. 2). Although the mutation is still unknown, it has been associated with a mild hypothalamic mitochondrial complex I dysfunction and a downregulation of the complex I assembly factor Ndufaf1 . Aberrances in several neuropeptidergic and neurotransmitter systems important for the regulation of food intake, particularly in the hypothalamus, have been documented, as well as signs of hypothalamic neuroinflammation and neurodegeneration.