Ageing Related Bone Loss
During ageing process our bones undergo changes, which make them predisposed to osteoporosis. Scientistsfrom Medical College of Georgia at Augusta University said that certain steroid hormones mayprovide a new understanding of ageing-related bone loss.
In previous study scientists found that histone deacetylase 3( HDAC3) can turn off the genes that force the bone marrow stem cells make and store fat instead of making bone. Since the level of HDAC3 declines with age, our bones become fragile.
Osteoporosis is a worldwide health problem which affects millions of people and costs billions yearly.
Researchersfrom Medical College of Georgia have focused their attention on steroid hormones, known as glucocorticoids. This study is of great importance, since glucocorticoids are natural steroids released in response to stress.
Level of glucocorticoids
The level of glucocorticoids increases with age and it correlates with bone loss. Besides, this group of steroids has potent anti-inflammatory properties. Therefore, they are widely prescribed to suppress immune response.And one of the side-effects of glucocorticoid treatment is osteoporosis.
In this study scientists discovered that by entering bone making cells (osteoblasts) glucocorticoidsbind to receptors that activate the genes responsible for fat storage. Thus, by inhibiting this glucocorticoid receptor one can prolong bone-making properties of a cell.
Scientists believe thatHDAC3 represses the transcription of the enzyme 11β-hydroxysteroid dehydrogenase type 1, which activates glucocorticoids that, in turn, initiate fatstorage.
To verify this theory, researchers conducted an experiment. Mice without steroid hormone receptor were placed in conditions imitating ageing process. Specifically, a diet with severe calorie restriction, which also leads to bone brittleness.
Scientists expected that receptor deficient animals would have less bone loss and marrow fat, due to the absence of steroid receptor. However, the results of experiment were controversial.
In a culture dish receptor deficient mice showed 80% less lipid storage and more bone matrix than in regular mice. But in vivo these mice had more marrow fat and less bone mass.
This means that inside the body, there’s some unknown factor in the bone marrow that causes different results.
This study may provide new opportunity for bone loss preventing therapy.