부산대학교 도서관

Based on the recent observation that human recombinant leptin (r‐Met‐hu‐leptin; metreleptin) may induce a profound alleviation of the complex symptomatology of patients with anorexia nervosa (AN), we examine the implications for our conceptualisation of this eating disorder. Hypoleptinemia as a core endocrine feature of AN serves as a central and peripheral trigger of tissue‐specific adaptations to starvation. In this narrative review, we argue that leptin deficiency may explain many of the puzzling features of this eating disorder. Weight loss can be viewed as a two‐step process, with only the second step entailing hypoleptinemia and thereby the entrapment characteristic of AN. We discuss the central and peripheral distribution of leptin receptors and consider possible functional implications of hypoleptinemia. We contrast the slow psychological recovery of patients with AN and of people who experienced starvation upon weight recovery with the rapid onset of improvements upon off‐label metreleptin treatment. Characteristics of the sex and age dependent secretion of leptin may contribute to the elevated vulnerability of young females to develop AN. Highlights: The development of hypoleptinemia may underlie the entrapment of patients with anorexia nervosa (AN), which in part can be conceptualised as a hormone deficiency disorder.Hypoleptinemia as a core endocrine feature of AN serves as a central and peripheral trigger of tissue‐specific adaptations to starvation.The continuous increase in leptin secretion throughout all stages of female puberty may explain the elevated risk for AN in females and the age manifestation range characteristic of this eating disorder. [ABSTRACT FROM AUTHOR]