Bone loss in models of leptin or leptin receptor deficiency has been linked with
lower osteoblast activity (9, 14), suggesting that cellular leptin resistance in obesity might reduce bone formation.
The Opotowski team, which found that
low vitamin A levels had as great an effect
lowering BMD as did high vitamin A levels, suggested that vitamin A deficiency may contribute to increased fracture risk by allowing bone matrix to grow faster than it can be mineralized.12 Indeed, although the net effect of vitamin A is to stimulate osteoclasts and slow the growth of
osteoblasts, vitamin A also causes
osteoblasts to secrete a variety of enzymes and other proteins that are important to bone mineralization, including osteocalcin, which is a protein that plays a direct role in attracting and binding calcium within the bone matrix.6 By slowing the growth of the matrix but increasing the rate at which it is mineralized, adequate vitamin A helps to ensure sufficient bone density.