The anorectic phenotype of the anx/anx mouse is associated with hypothalamic dysfunction

Abstract

The anorectic anx/anx mouse, mimicking the core characteristics of anorexia nervosa (AN), i.e., reduced food intake, emaciation, and premature death, is an interesting and useful model for studies of mechanisms involved in the regulation of food intake as well as the development and maintenance of AN. The anorexia (anx) mutation arose spontaneously at the Jackson Laboratory in 1976 and has 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, a gene located in the mapped interval. 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 and pancreatic dysfunction.