Fortunately only one adrenergic receptor, the β2 adrenergic receptor (Adrβ2), is expressed in osteoblasts and mice lacking this receptor have already been generated. These animals are not obese, are fertile, and have none of the metabolic abnormalities seen in ob/ob and db/db mice. Yet, they display an increase in bone formation and in bone mass that cannot be rescued by leptin ICV infusion. This experiment established genetically that the sympathetic nervous system, via Adrβ2, mediates leptin regulation of bone mass [1].
Cross-talk between bone cells includes chondrocytes and puts vitamin D into play
20/05/2008 in PhysiologyGenomic actions induced by the active form of vitamin D, 1α25-dihydroxyvitamin D3 [1,25(OH)2D3] are crucial for normal bone metabolism, mainly because they regulate active intestinal calcium transport. To evaluate whether the vitamin D receptor (VDR) has a specific role in growth-plate development and endochondral bone formation, the group of G Carmeliet [1] investigated mice with conditional inactivation of VDR in chondrocytes. Surprisingly, growth-plate chondrocyte development was not affected by the lack of VDR. Yet vascular invasion was impaired, and osteoclast number was reduced in juvenile mice, resulting in increased trabecular bone mass. In vitro experiments confirmed that VDR signaling in chondrocytes directly regulated osteoclastogenesis by inducing RANKL expression by these cells.
A significant portion of milk calcium comes from the mother¿s skeleton, and lactation is characterized by rapid bone loss. The most remarkable aspect of this bone loss is its complete reversibility, and the time following weaning is the most rapid period of skeletal anabolism in adults. Despite this, little is known of the mechanisms by which the skeleton repairs itself after lactation. In a recent study [1], the authors examined changes in bone and calcium metabolism defining the transition from bone loss to bone recovery at weaning in mice.
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β-catenin age BMD bone bone density bone density test bone formation bone fracture bone loss bone marrow bone remodeling bone resorption bone strength breast cancer calcium cardiovascular cardiovascular disease cell cell bone marrow cholesterol Clinical data diabetes disease epidemiology fracture fracture risk FRAX heart heart disease hip fracture mesenchymal stem cells neuromedin U osteoblast osteoblast differentiation osteoclast osteoporosis osteoprotegerin osterix ovariectomy RANKL residual lifetime risk risk factors sclerotin survival weight loss