1,25(OH) 2 D 3 ameliorates palmitate-induced lipotoxicity in human primary osteoblasts leading to improved viability and function.
Al Saedi A., Myers DE., Stupka N., Duque G.
Laboratory Study, published in Bone (2020) — 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
- Laboratory Study
- Journal
- Bone (2020)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 33011427
- DOI
- 10.1016/j.bone.2020.115672
Abstract (original English)
Contributing to bone loss with aging is a progressive reduction in osteoblast number and function leading to decreased bone formation. In aging bone, mesenchymal stem cells decrease in number and their differentiation potential into osteoblasts is reduced. Instead, there is a shift towards adipogenic differentiation and increased lipid accumulation in the marrow of osteoporotic bones. Bone marrow adipocytes produce palmitic acid (PA), a saturated fatty acid, which is toxic to osteoblasts in vitro. Vitamin D (1,25(OH) 2 D 3 ) stimulates osteoblastogenesis and has known anti-apoptotic effects on osteoblasts, as such it may protect human primary osteoblasts from PA-induced lipotoxicity. Here, the effects of PA (250 μM) or 1,25(OH) 2 D 3 (10 -8 M), alone or in combination, on osteoblast differentiation and mineralization, viability and autophagy were investigated. In PA-treated osteoblasts, 1,25(OH) 2 D 3 ameliorated the decrease in the mRNA transcript abundance of representative palmitoylation (ZDHHC1, ZDHHC2 and ZDHHC12) and osteogenic (alkaline phosphatase and osteocalcin) genes. Collectively these gene regulate signaling pathways pertinent to osteoblastogenesis. In osteoblasts treated with PA and 1,25(OH) 2 D 3 , the capacity to undergo differentiation and mineralization was recovered and cell viability was increased when compared to osteoblasts treated with PA alone. 1,25(OH)
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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