Although population-based studies have suggested a consistent inverse relationship between AD and increasing family size, this does not seem to be explained by a straightforward increased exposure to a single environmental pathogen. The effect seen with early day care, endotoxin and animal exposure may be due to a nonpathogenic microbial stimulus of a chronic or recurrent nature. This would also explain the risk increase associated with antibiotic use. Caution should prevail in the prescribing of antibiotics early in life, especially in children with a family history of AD. Larger well-designed pragmatic trials on probiotics and the prevention and treatment of AD are now needed to inform whether such interventions should be used in routine clinical practice.
For many years it has been recognized that sex steroids have profound effects on bone metabolism. The current perception is that estrogen decreases bone resorption and androgen increases bone deposition. To investigate the potential for androgens to directly modulate bone resorption, we have examined avian osteoclast and human and mouse osteoclast-like cells for androgen responsiveness. There was a dose-dependent decrease in resorption activity in response to ␣-dihydrotestosterone (␣-DHT), -DHT, testosterone, or the synthetic androgen RU1881. This decrease was blocked by cotreatment with the specific androgen antagonist hydroxyf lutamide. Further examination of avian osteoclasts revealed that the cells exhibited specific and saturable nuclear binding of tritiated RU1881 and that ␣-DHT stimulated the activity of the androgen response element as measured by using a chloramphenicol acetyltransferase reporter plasmid. In addition, avian osteoclasts responded to androgen treatment with elevated production and secretion of transforming growth factor , a well documented response to androgen exposure in other cell systems. Treatment with either ␣-DHT or -DHT for 24 hours resulted in a significant dosedependent decrease in secretion of cathepsin B and tartrateresistant acid phosphatase. This response to -DHT, a stereoisomer of ␣-DHT that is inactive in other androgen receptor-dependent systems, supports the hypothesis that the osteoclast androgen receptor has unusual ligand-binding properties. Taken together, these results confirm the presence of functional androgen receptors in these cells and support the conclusion that osteoclasts are able to respond directly to androgens in vitro and thus are potential androgen target cells in vivo.Androgens have long been recognized to play an important role in the normal development and physiology of bone and have profound influences on bone development and metabolism (1). The evidence published to date suggests that androgens exert their effects on bone metabolism through stimulation of bone formation by both indirect and direct effects on bone-forming osteoblasts derived from both males and females (2-4). Although the incidence of hip fractures in elderly men is less than in elderly women (17% in men versus 32% in women), osteoporosis in men is still a significant health problem with an aging population (5). Decreased androgen levels have been linked to lower bone density in men, yet there has been no definitive proof that there is a link between lower androgen levels and the increase in the incidence of hip fracture (6). There is, however, a strong correlation between hypogonadism in elderly men and hip fracture and spinal osteoporosis (5, 6). Although one study of males matched for age, race, and lifestyle has shown a direct correlation between hip fracture incidences and lower gonadal steroid levels (7), it has proven difficult in other studies to correlate serum androgen levels and risk for osteoporosis in elderly men, and it is likely that there are many other fa...
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.