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A group of steroid hormones could provide new insight into the bone loss and deterioration that occurs with aging, protein histone deacetylase 3, HDAC3, turns off the genes that encourage the stem cells in our bone marrow to make and store fat instead of making bone. As HDAC3 levels decrease naturally with age, bones become less dense and easily breakable.
Looking at a group of steroid hormones known as glucocorticoids, which our bodies naturally have in circulation as a response to different stresses to help quiet the immune response, when these hormones enter bone cells, osteoblasts that make bone bind to a receptor that activates the expression of genes related to fat storage.
To get that effect of bone loss and increased marrow fat when you lose HDAC3, glucocorticoids must be present. Releasing glucocorticoids in response to various stimuli is a natural thing that body does, circulating glucocorticoid levels increase with age.
As with a lot of chemicals in the body, too much and not enough of something can be bad. While glucocorticoids occur naturally in the body, they are also used in various immune-suppressive therapies, many of which have osteoporosis as a side effect.
Researchers studied mice without receptors for the steroid hormones. The mice were placed on a calorie-restricted diet to stimulate the aging process which also has been shown to result in lower bone density and increased marrow fat. Extreme caloric restriction, such as with anorexia nervosa, can also lead to weak and brittle bones.
When looking at the bone cells in a culture dish, the receptor deficient mice show less lipid storage than regular mouse models of aging. They also showed more bone matrix, which is the cause of bone formation. Examination of tibia and femur in a living animal showed the receptor deficient mice actually had more marrow fat and lower bone mass.
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