1,25(OH)2D3 inhibits bone marrow adipogenesis in senescence accelerated mice (SAM-P/6) by decreasing the expression of peroxisome proliferator-activated receptor gamma 2 (PPARgamma2).
Duque G., Macoritto M., Kremer R.
Animal Study, published in Exp Gerontol (2004) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Exp Gerontol (2004)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 15036392
- DOI
- 10.1016/j.exger.2003.11.008
Abstract (original English)
Senile osteoporosis is the endpoint of a continuum that starts after the third decade of life when peak bone mass is attained and then is followed by a progressive and irreversible decline in bone mass. One of the mechanisms that could explain this is the increasing levels of adipogenesis in bone marrow seen with increasing age, probably due to alterations in the differentiation of mesenchymal stem cells (MSC). Senescence accelerated mice (SAM-P/6) constitute an accepted model for senile osteoporosis since their loss of bone mineral density is clearly due to high levels of adipogenesis and a deficit in osteoblastogenesis. It is known that MSC expressing a ligand-activated transcription factor known as peroxisome proliferators-activated receptor gamma 2 (PPARgamma2) are committed to differentiate into adipocytes. The regulation of PPARgamma2 activation may play a role in the control of adipogenic differentiation of MSC and thus contribute to their differentiation into osteoblasts in order to form new bone. Our previous studies have shown that the active form of vitamin D (1,25(OH)(2)D(3)) plays a role as a bone forming agent because it induces osteoblastogenesis and inhibits adipogenesis in bone marrow of SAM-P/6 mice. To elucidate the role of 1,25(OH)(2)D(3) on the expression of PPARgamma2 we treated 4-month old SAM-P/6 mice with 1,25(OH)(2)D(3) (18pmol/24 h) or vehicle during
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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