[Menopause, obesity, and bone status].

: Recent studies indicate that obesity is not a risk factor of osteoporosis. On the contrary, increased adipose tissue mass may have a protective effect against osteoporosis. This suggests that the positive influence of adipose tissue on bone tissue may be a consequence of the boost in load on the bone tissue, leading to increased bone anabolism. It may also be connected with changes frequently occurring in postmenopausal women in the formation of some osteotropic factors, mainly hormones such as estrogens, androgens, calciotropic hormones, somatotrophin axis hormones, leptin, and melatonin. The antiresorption effects of the above hormones on the bone are to a considerable extent executed through the RANKL/RANK/OPG system (receptor activator of nuclear factor-kB ligand/receptor activator of nuclear factor-kB/osteoprotegerin), the principal signaling pathway through which osteoblasts regulate the rate of the activated osteoclast pool. This effect may be achieved through a direct effect on the expressions OPG and/or RANKL in osteoblasts and marrow stroma cells and/or indirectly through cytokines, mainly interleukins (IL)-1 and -6, tumor necrosis factor-alpha(TNF-alpha), macrophage colony-stimulating factor (M-CSF), and tumor necrosis factor-beta (TNF-beta).