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Prostaglandins Leukotrienes and Essential Fatty Acids 2003-Jun

Protective role of n-3 lipids and soy protein in osteoporosis.

Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
Saite tiek saglabāta starpliktuvē
Gabriel Fernandes
Richard Lawrence
Dongxu Sun

Atslēgvārdi

Abstrakts

It is well established that bone loss due to estrogen deficiency after menopause is greater in women consuming higher quantities of animal protein than in women consuming vegetable protein, particularly soy protein. Besides the dietary protein source altering bone loss, it has also been postulated recently that the source of a higher n-6/n-3 ratio in dietary oils is implicated in causing osteoporosis. Both animal and human studies have indicated that an increased intake of n-6 fatty acids from vegetable oils elevates prostaglandin E(2) levels as well as pro-inflammatory cytokines such as IL-1, IL-6 and TNF-alpha. Interestingly, it has been found that lack of estrogen also increases the production of these cytokines by immune cells and thereby activates osteoclasts during the peri-menopausal period. We speculated that the use of n-3 fatty acids and soy protein, which are known to act as anti-inflammatory and down regulate pro-inflammatory cytokines, may also protect against bone loss by decreasing osteoclast activation and bone resorption. Similar to the results of others, our ongoing studies indeed show that the bone loss in ovariectomized mice is significantly attenuated by feeding diets enriched with either fish oil or soy protein when compared to corn oil and casein-fed mice. One of the mechanisms appears to be decreasing the activation of receptor activator of NF-kappaB ligand (RANKL) on T cells, which has been found to increase osteoclast activation along with increasing pro-inflammatory cytokines in OVX mice. Since hormone replacement therapy has been found to cause adverse effects, further both animal and human studies are required with moderate soy protein and fish oil supplements in understanding the mechanisms involved in altering immune function and bone loss during menopause in women and aging in men.

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