Background: Anorexia nervosa is a widely prevalent eating disorder that often leads to life-threatening complications. Since it mostly concerns females, many authors have focused on studying the reproductive system in anorexic women. Recently discovered telocytes may give a new insight into the pathophysiology of gynecological complications in these patients.

Material and Methods: We adopted an animal model of anorexia nervosa induced by voluntary physical activity. Sixteen female Wistar rats were divided into two groups: control and activity-based anorexia. When the weight loss of activity-based anorexia (ABA) rats reached 25% animals were euthanized. Size and weight measurements as well as histopathological analysis of the reproductive organs were performed. Additionally, we used immunohistochemical staining for detection of telocytes.

Results: Telocytes were identified in uteri of anorectic rats but no diff erences were observed when compared to the control group. Nevertheless, in the ABA group the weight of the uteri and the number of follicles in the ovaries decreased significantly.

Conclusions: Our rat model of anorexia nervosa mimics the effects of this eating disorder that occur in the female reproductive system since we reported ovarian dysfunction and uterine involution in the experimental animals. It supports its potential role in the further studies of anorexia pathophysiology and treatment possibilities.

Eating disorders are a heterogeneous group of diseases affecting mainly young people in devel-oped countries. Among them, anorexia nervosa (AN) is the one with the highest mortality, up to five times higher compared to healthy individuals. The etiology of this medical condition is complex and still un-certain. However, disturbances of the autonomic nervous system (ANS) and increased lipolysis resulting in a decrease of the adipose tissue volume are common findings among AN patients. Since ANS is directly connected to adipocyte tissue, thus significantly affecting the body’s metabolic homeostasis, we suspect that this relationship may be a potential pathophysiological underpinning for the development of AN. In this narrative review, we have analyzed scientific reports on ANS activity in AN considering different phases of the disease in humans as well as animal models. Due to the different effects of the disease itself on the ANS as well as specific variations within animal models, the common feature seems to be dysre-gulation of its function without the identification of one universal pattern. Nonetheless, higher norepi-nephrine concentrations have been reported in adipocyte tissue, suggesting local dominance of the sym-pathetic nervous system. Further studies should explore in depth the modulation of sympathetic in adipose tissue factor and help answer key questions that arise during this brief narrative review.

Anorexia nervosa (AN) is an eating disorder characterized by distinct etiopathogenetic concepts that are gradually being linked together to unravel the dominant pathophysiological pathways underlying the disease. Excessive food restrictions, often accompanied by over-exercise and undertaken to lose weight, lead to the development of numerous complications. The biological concept of neurohormonal dysfunc-tion in AN seems incomplete without demonstrating or excluding the role of the enteric nervous system (ENS). Using an animal model of activity-based anorexia (ABA), we conducted the preliminary assess-ment of the ENS structure. Here we show, in preparations stained by immunohistochemistry with anti- ChAT, anti-NOS, anti-PGP 9.5, anti-c-fos, and anti-TH antibodies, a lower density of cholinergic and nitrergic nerve fibers as well as reduced neuronal activity in myenteric plexus. Such structural and functional damage to the ENS may be responsible for a number of gastrointestinal symptoms that worsen the course of the disease. In addition, we expanded the study to address the unresolved issue of mechanical and thermal pain sensitivity in AN. The Von Frey and hot plate tests revealed, that in ABA animals, the pain threshold for mechanical stimulus decreases while for thermal increases. In this way, we have sig-nificantly supplemented the background of AN with potentially observable nervous system changes which may influence the evolution of the therapeutic approach in the future.