Bone mineral density in children and adolescent girls with anorexia nervosa in Japan.

BACKGROUND: The correlation between reduced bone mineral density (BMD) and the disease anorexia nervosa (AN) has long been established. The aim of the present study was to examine the relationship in more detail, particularly focusing on the increasing incidence of the disease occurring in adolescent patients. METHOD: Twenty-four girls diagnosed with AN were enrolled in the study. All subjects ranged in age from 11.1 to 15.5 years, with an average age of 13.5 years. The BMD of lumbar spines and femoral necks were measured. All the values for BMD at admission were expressed as means +/- SD and patients with and without menarche were separately investigated. RESULTS: The average BMD of lumbar spines at the time of admission was -0.51 SD in total. However, the average BMD of patients without menarche was -1.28 SD, which was significantly lower than the -0.16 SD on average in patients with menarche. As a whole the BMD of femoral necks at admission tended to be lower than that of lumbar spines. Similarly, it was lower in patients without menarche (-1.7 SD on average) than in those with menarche (-0.77 SD on average). CONCLUSIONS: BMD was lower in children and adolescent AN patients without menarche, and such a tendency was more significant at the femoral neck region. In child AN cases without menarche, the BMD, especially at the femoral neck, needs to be measured, and later recovery should be monitored closely over a long period.

The chromatin-remodeling complex WINAC targets a nuclear receptor to promoters and is impaired in Williams syndrome.

We identified a human multiprotein complex (WINAC) that directly interacts with the vitamin D receptor (VDR) through the Williams syndrome transcription factor (WSTF). WINAC has ATP-dependent chromatin-remodeling activity and contains both SWI/SNF components and DNA replication-related factors. The latter might explain a WINAC requirement for normal S phase progression. WINAC mediates the recruitment of unliganded VDR to VDR target sites in promoters, while subsequent binding of coregulators requires ligand binding. This recruitment order exemplifies that an interaction of a sequence-specific regulator with a chromatin-remodeling complex can organize nucleosomal arrays at specific local sites in order to make promoters accessible for coregulators. Furthermore, overexpression of WSTF could restore the impaired recruitment of VDR to vitamin D regulated promoters in fibroblasts from Williams syndrome patients. This suggests that WINAC dysfunction contributes to Williams syndrome, which could therefore be considered, at least in part, a chromatin-remodeling factor disease.