Introduction: Young women and girls with anorexia nervosa (AN) suffer from abnormalities in melatonin (MEL) secretion, especially in the nocturnal phase. This is paralleled by a considerable bone mass loss and abnormalities of bone metabolism. As melatonin has been implicated in playing a role in inducing osteoporosis and that the effect could be mediated by the RANKL/RANK/OPG system, we decided to investigate the potential associations between MEL and bone status in girls with AN. Aim: To evaluate the relationship between MEL, bone metabolism (as assessed by serum levels of bone turnover markers [OC and CTx]), and OPG and sRANKL in girls with AN.
Material and methods: A total of 57 girls with AN and 13 healthy girls, between 13 and 18 years of age, were enrolled in the study, and we evaluated BMI, fasting levels of OC, CTx, OPG and sRANKL, and levels of MEL (fasting levels and the levels at 2 a.m., at which time the secretion of the hormone peaks).
Results: We found a significantly increased mean serum level of MEL at 2 a.m. and an increased amplitude between nocturnal and morning levels of the hormone in girls with AN. We also showed a considerable suppression of the mean OC and CTx levels and an increase in serum OPG and RANKL levels paralleled by a significantly reduced OPG/sRANKL ratio. The changes in the MEL levels at 2 a.m. showed a statistically significant negative correlation with levels of the bone markers and a positive correlation with sRANKL. The changes in the amplitude between the nocturnal and morning levels of MEL showed a negative correlation with CTx levels and the OPG/sRANKL ratio.
Conclusions: Our results indicate that the abnormalities of bone metabolism in girls with AN are associated with changes in the nocturnal levels of MEL with RANKL appearing to play an important role in this mechanism. The increased amplitude between the nocturnal and morning levels of MEL may adversely affect the bone tissue in girls with AN with the effect most likely resulting from influences on the OPG/RANKL balance.
(Pol J Endocrinol 2010; 61 (1): 117-123)