Leptin inhibits bone formation through a hypothalamic relay: a central control of bone mass

Article Abstract:

Central control of bone mass is discussed in view of leptin's having been found to inhibit bone formation via a hypothalmic route. Gonadal failure brings on bone loss, but obesity works against it, raising the possibility that bone mass, body weight and gonad function are regulated by common pathways. Leptin-deficient and leptin receptor-deficient mice that are obese and hypogonadic have been studied. Both have greater bone formation than normal leading to high bone mass in spite of hypercortisolism and hypogonadism. LIttle is known about genetic control of bone formation by osteoblasts.

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Continuous expression of Cbfa1 in nonhypertrophic chondrocytes uncovers its ability to induce hypertrophic chondrocyte differentiation and partially rescues Cbfa1-deficient mice

Article Abstract:

The endochondral ossification involves chondrocyte hypertrophy, which may be mediated by the Cbfa1 gene. Results from Cbfa1-deficient mice identify that Cbfa1 is indeed a hypertrophic chondrocyte differentiation factor and in addition, it regulates osteoblast differentiation.

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A Cbfa1-dependent genetic pathway controls bone formation beyond embryonic development

Article Abstract:

Research has found that a Cbfa1-dependent genetic pathway controls bone formation beyond embryonic development. Cbfa1 is a transcriptional activator of osteoblast differentiation at the time of embryonic development and is expressed in differentiated osteoblasts after birth. To find out whether Cbfa1 has a role in bone formation, transgenic mice that overexpress Cbfa1 DNA-binding domain were developed. Molecular analyses showed that expression of genes expressed in osteoblasts and encoding bone ECM proteins is almost absent in transgenic mice. Cbfa1 is the first transcriptional activator for bone formation found so far and it regulates its own promoter's activity positively. Developmentally important genes can be important in controlling physiological processes after birth too. Bone formation here is taken to be postnatal bone extracellular matrix (ECM) deposition by differentiated osteoblasts.

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