Endocrine Abstracts

That obesity protects mammals from osteoporosis led us to show in the past that bone remodeling, and thereby bone mass, is regulated by the adipocyte-derived hormone leptin via a central relay and the sympathetic nervous system. To test whether in response to this regulation bone could exert a feedback control of energy homeostasis we performed a functional genetic screen in mice designed to identify genes expressed specifically in osteoblasts, encoding signaling molecules and...

The process of bone remodelling enables the conservation of an optimal bone mass and properties during adult life. Recent evidences, based on genetic and pharmacological data, revealed that this process is under the control of hypothalamic and neuronal signals released by sympathetic nerves in the bone microenvironment. The implication of these findings is that bone remodelling can be considered as a classical homeostatic process, coupled and fully integrated with other endocr...

In contrast to traditional ideas that loss of estrogens at menopause is the seminal mechanism of osteoporosis, bone loss begins as early as the early part of the third decade in both women and men; substantial trabecular bone loss occurs in sex steroid sufficient young adult women and men; and after the first few years of accelerated bone loss in postmenopausal women, bone mass and strength decline in both sexes at the same rate. Consistent with these clinical observations, me...

Osteoporosis is a common, age-related disease with a strong genetic component. Mutations in the low-density lipoprotein receptor-related protein 5 (LRP5) gene are known to cause rare bone-related syndromes including loss-of-function mutations with decreased bone mineral density (BMD) and gain-of-function mutations with high bone mass. The initial discovery of lipoprotein involvement in bone metabolism was surprising, but revealed a strong regulatory pathway by the Wnt-signalli...