**1. Introduction**

Anorexia nervosa (AN) is a serious mental disorder characterized by self-induced starvation and excessive weight loss, fear of weight gain, body image concerns and food aversion [1]. Psychiatric comorbidities are common in patients with AN, as well as an increased mortality rate due to medical complications and suicide [2,3]. Previous research has identified numerous factors involved in the etiology of AN, where psychological, sociocultural and biological factors contribute to both the onset and maintenance of this disorder [4,5]. Recently, neurobiological alterations have been proposed as major factors contributing to AN [6]. Specifically, various studies have begun to employ neuroimaging techniques to elucidate the underlying pathophysiology and neurobiological substrate of AN [7–10]. Altered neural activity is observed throughout the brain in patients with AN, including cortical- and subcortical regions [7,11,12]. Based on neuroimaging investigations, theories have been proposed to explain the contribution of aberrant brain function to the development and maintenance of AN. For example, hyperactivity in cognitive control networks and a cooccurring reduction in motivational responses to food has been proposed as a core neural mechanism underlying the development of AN [5,12–14]. In contrast, reduced somatosensory and insula processing of taste stimuli may relate to a failure to accurately recognize hunger signals [15,16]. However, due to methodological differences

between neuroimaging studies, as well as a paucity of studies employing a longitudinal design to differentiate between the state and trait, the exact neurobiological mechanisms of AN remain unclear. The aim of this review is to provide a narrative overview of recent studies investigating alterations in brain function related to disorder-specific stimuli in patients with AN and to provide a better characterization of the pathophysiological mechanisms underlying AN. Specifically, we focused on neuroimaging studies employing experimental designs drawing on symptom provocation to assess neural aberrations associated with AN. Symptom provocation has been extensively analyzed in patients with AN since the advent of fMRI-techniques [17] and has played an important role in the elaboration of neurobiological theories of AN. The following section will outline results from previous neuroimaging investigations grouped by stimulus type and relate these findings to current approaches examining neuroanatomical biomarkers of AN. Specifically, we describe studies investigating the following: (1) the responsivity to food-related stimuli, (2) hunger, (3) body image, (4) emotional processing and (5) interoceptive processing.
