By A. Kalsbeek, E. Fliers, M.A. Hofman, D.F. Swaab, E.J.W. van Someren and R.M. Buijs (Eds.)
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2003). The hypothalamo–pituitary–adrenal and –thyroid axes remain largely intact in PWS, and prolactin and cortisol levels are generally normal (Swaab, 2004). Leptin is a satiety factor that is produced by fat cells and acts on the infundibular nucleus and other hypothalamic areas in order to inhibit food intake and was, therefore, presumed to be involved in obesity in PWS. , 1999). In order to see whether an increased activity of neuropeptide-Y (NPY) neurons in the infundibular nucleus might explain the eating disorder in PWS patients, we determined the amount of NPY in the infundibular nucleus immunocytochemically, and NPY mRNA, by means of an image analysis system, in PWS cases, nonsyndromic obese patients and controls.
Fig. 15. Examples of staining of hypocretin-IR cell bodies in the lateral hypothalamus of an adult control subject #02-076 (A), an adult Prader–Willi patient #91-058 (B), a control infant #97-153 (C) and a Prader–Willi infant #99-079 (D). There was no significant difference in the intensity of staining and the distribution pattern. , with permission). , 2000, 2001). , 2000; Van de Pol, 2000) argues in favor of some type of neuronal degeneration. However, Peyron et al. (2000) could not confirm the presence of hypothalamic gliosis in narcolepsy.
In conclusion, so far hypothalamic research has revealed an intact NPY/AGRP and GHRH system in PWS syndrome that is inhibited in a normal way by obesity, but the number of oxytocin-expressing neurons in the PVN is clearly diminished. The hypothalamic hypocretin(orexin) system in PWS Narcoleptic patients with cataplexy have a general loss of hypocretin (orexin) in the lateral hypothalamus, possibly due to an auto-immunemediated degeneration of the hypocretin neurons. Obesity is one of the frequent symptoms in narcolepsy (see before).
