155 Endocrine and Metabolic Alterations following Deep Brain Stimulation in Anorexia Nervosa Appetite regulating hormones, gut peptides and adipokines At baseline, leptin in our patients was low (3.75±0.73 ng/mL), as would be expected in AN patients (10, 11). We found a mean increase of leptin at the other time points, but this was not significant due to a large variability. On an individual level, a numerical increase in leptin was seen in the two subjects that also responded to DBS with significant weight increase (see supplement 2). An increase in leptin levels would be in line with the hypothesis that leptin levels are associated with appetite regulation and fat mass and thus normalize after treatment and weight gain (22). In our study we found no significant changes in adiponectin levels over time. In human (non-AN) studies administration of adiponectin seems to reduce body weight by various mechanisms, and/ or by reducing food intake, increasing energy expenditure and enhancing fatty acid oxidation (27). It could be hypothesized that this hyperadiponectinaemia could contribute to the pathogenesis of AN (28). However, the role of adiponectin in AN remains unclear and our results were insufficient to support any hypothesis. Catecholamines and dopamine We assessed plasma levels of dopamine, noradrenaline and adrenaline, but did not find any significant changes over time, although in the individual charts there seems to be a downward trend in dopamine as well as noradrenaline (see supplement 2) over time. These decreases seem most prominent in our weight-responders which is supportive of our hypothesis that improvement of eating disorder pathology, in this case weight gain, is associated to normalization of epinephrines and dopamine. Fatty acids Fatty acid changes during DBS treatment did not reach significance. Given the widespread potential significance of lipids in brain structure/function and inflammatory regulation (29-38), this may be because of power issues. Of interest was the numerical increase in lipid peroxidation index, apparently mostly in weight-responders, which deserves follow-up in larger studies in AN. Limitations A major limitation of this study is of course the small sample size. Therefore it was not possible to statistically correlate endocrine and metabolic parameters to weight change or severity of symptoms. As stated in the introduction, AN is characterized by a wide variety of endocrine and metabolic alterations, and the causality of these alterations is hard to establish. Furthermore, this study consisted of a specific subgroup of AN patients, which all were extremely and chronically ill, with major acute and long-term complications of severe and enduring malnutrition. Furthermore, the population we studied was heterogeneous due to a variety of comorbid conditions. Many endocrine parameters do have a diurnal rhythm and the levels of gonadotrophins are highly dependable on the pase of the menstrual cycle. Therefore, we are cautious in interpreting
RkJQdWJsaXNoZXIy MjY0ODMw