AN,BN,VHM

The ventromedial hypothalamus (VMH),  by contrast,is criticalin evaluating the organism's
 energy balance. The VMH contains insulin-sensitive  cells and is able to integrate information about the status of peripheral energy stores. This
 function is mediated,in part, by secretion of leptin and other neuropeptides. The hypothal-
 amus is anatomically close to the pituitary gland, which secretes hormonally active
 neuropeptides involved in energy regulation of the body such as thyroxine, growth
 hormone (GH), cortisol, and leptin.In AN,there is usually an excess of GH activity,
 whereas the insulin-like growth factor I is often found to be reduced. GH interacts in
 complex ways with somatostatin, and may also be influenced by leptin and ghrelin secre-
 tion (the latter being a gastric somatotropin-stimulating hormone). Other neuropeptides
such as orexin and neuropeptide Y are involved in regulation of food intake. Neuropeptide
Y has been found elevated in the cerebrospinal fluid (CSF) of patients with BN. Stress
increases the level of neuropeptide Y, which may cause abdominal fat deposition. Moreover,
cholecystokinin, Wトich is secreted by the gut to signal satiety,is decreased in BN. This
reduction in satiety signalling may,therefore, be part of the pathology of binge eating.
   Interestingly,in terms of the AN phenotype,the VMH is not only involved in the regu-
lation of food intake. The VMH also controls female sexual receptivity, which may
explain why patients with AN experience reduced sexual interest when starving. Also,
hypertrichosis, amenorrhoea and a more male-type physiognomic phenotype are the
result of complex dysregulations of the neuroendocrine circuits, which remit upon
restoration of a sufficient amount of body fat. This suggests that most pathophysiological
mechanisms in AN and BN are the result rather than the cause of the disorder.
  Similarly, at the anatomical level, chronic reduction of food intake to the point of
starvation may lead to cortical atrophy and ventricular enlargement. This is believed to
be a consequence,rather than cause of eating disorders, and partly remits following
weight gain.