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 (PPARγ2)

Duque, Gustavo; Macoritto, Michael; Kremer, Richard

doi:10.1016/j.exger.2003.11.008

Cited by 70 publications

(62 citation statements)

References 21 publications

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“…Treatment of adult male C57Bl6 mice with PPARg inhibitors increases bone mass and stimulates bone formation Nine-month-old C57BL/6 male mice were treated for 6 weeks with a daily ip injection of 30 mg/kg BADGE in 15% DMSO alone or in combination with a previously validated (12,17) anabolic dose of 1,25(OH) 2 D 3 administered by subcutaneous pump at a dose of 18 pm/d, using vehicle-treated mice as control. Faxitron X-ray (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Percentage of marrow fat content was calculated as fat volume/total volume (FV/TV) using haematoxylin/eosinstained sections as previously described. (16,17) Statistical methods All results were expressed as the mean AE standard error (SE). Differences of the structural and static parameters of bone histomorphometry between different groups of mice were determined using Levene's test for homogeneity of variances and the unpaired t test for equality of means.…”

Section: Quantification Of Marrow Fatmentioning

confidence: 99%

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Pharmacological inhibition of PPARγ increases osteoblastogenesis and bone mass in male C57BL/6 mice

Duque

Vidal

et al. 2012

Journal of Bone and Mineral Research

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Infiltration of bone marrow with fat is a prevalent feature in people with age-related bone loss and osteoporosis, which correlates inversely with bone formation and positively with high expression levels of peroxisomal proliferator-activated receptor gamma (PPARg). Inhibition of PPARg thus represents a potential therapeutic approach for age-related bone loss. In this study, we examined the effect of PPARg inhibition on bone in skeletally mature C57BL/6 male mice. Nine-month-old mice were treated with a PPARg antagonist, bisphenol-A-diglycidyl ether (BADGE), alone or in combination with active vitamin D (1,25[OH] 2 D 3 ) for 6 weeks. Micro-computed tomography and bone histomorphometry indicated that mice treated with either BADGE or BADGE þ 1,25(OH) 2 D 3 had significantly increased bone volume and improved bone quality compared with vehicle-treated mice. This phenotype occurred in the absence of alterations in osteoclast number. Furthermore, the BADGE þ 1,25(OH) 2 D 3 -treated mice exhibited higher levels of unmineralized osteoid. All of the treated groups showed a significant increase in circulating levels of bone formation markers without changes in bone resorption markers, while blood glucose, parathyroid hormone, and Ca þ remained normal. Furthermore, treatment with BADGE induced higher levels of expression of vitamin D receptor within the bone marrow. Overall, treated mice showed higher levels of osteoblastogenesis and bone formation concomitant with decreased marrow adiposity and ex vivo adipogenesis. Taken together, these observations demonstrate that pharmacological inhibition of PPARg may represent an effective anabolic therapy for osteoporosis in the near future. ß

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Section: Resultsmentioning

confidence: 99%

Section: Quantification Of Marrow Fatmentioning

confidence: 99%

Pharmacological inhibition of PPARγ increases osteoblastogenesis and bone mass in male C57BL/6 mice

Duque

Vidal

et al. 2012

Journal of Bone and Mineral Research

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“…A Dvitamin közvetlenül csontsejtekre gyakorolt hatása rendkívül összetett, az osteoblastokon és az osteoclastokon is érvényesül. Az aktív Dvitamin növeli a RANKL mennyiségét, ezen keresztül fokozza az osteoclastok érését, ugyanakkor gátolja a kifejlett osteoblastok apoptózisát, fokozza a Cbfa1 és a BMP2,6 átíródását [73], sőt gátolja az adipogenezist a PPARgamma expresszióján és aktiváló dásán keresztül [74], valamint fokozza a csontképzést [75]. Dvitaminhiányban ugyanakkor a gyors csont anyagcseréjű csontvesztés uralja a képet, ami döntően a másodlagos PTHemelkedés következménye.…”

Section: D-vitamin-hiány Hatása a Csontanyagcserére Dr Szekeres Lászunclassified

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et al. 2012

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A Dvitamin anyagcseréje egyedülálló az emberi szer vezetben. Hatása szerteágazó, szinte minden szervrend szerben érvényesül. Hiánya az egyik legnagyobb egész ségügyi probléma a civilizált világban. A probléma megoldása széles körű összefogást sürget. Ezt felis merve, a Dvitaminhiány következményeivel küzdő legnagyobb magyarországi orvostársaságok közös kon szenzust dolgoztak ki a Dvitaminhiány jelentőségéről, felismerési lehetőségeiről, a prevenció és a kezelés java solt módjairól. A társaságok szakmai irányelvei mellett ennek a konszenzusnak az eredménye iránymutatást ad a gyakorló orvosoknak a Dvitaminhiány megelőzésé hez és kezeléséhez. Emellett szeretné ráirányítani a szak mai döntéshozók és a laikus közönség fi gyelmét a prob léma fontosságára.

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“…In porcine mesenchymal stem cells (MSC), calcitriol stimulates adipocytic differentiation and increases the concentrations of mRNA encoding peroxisome proliferator-activated receptor gamma (PPARɤ), lipoprotein lipase, and adipocyte-binding protein 2 [123]. In the MSC of the senescence-accelerated mice (SAM-P/6), however, calcitriol inhibits bone marrow adipogenesis by decreasing the expression of PPARɤ2 and thus contributes to their differentiation into osteoblasts to form new bone [124]. Calcitriol and its analogs were reported to inhibit the adipogenesis and PPARɤ2 gene transcription in the murine 3T3-L1preadipocyte cell line [125][126].…”

Section: Role Of Vitamin Dmentioning

confidence: 99%

Vitamin D and Obesity

Lương¹,

Nguyễn²

2012

Med Chem

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Objective: The prevalence of overweight and obesity is considered an important public issue in the United States and is increasing among both children and adults. There is evidence of aberrations in the vitamin D-endocrine system in obese subjects. Therefore, we will review the role of vitamin D in the adipose tissue. Methods Conclusion:Vitamin D plays a role in the regulation of adipose tissue. Obese individuals may need higher doses of vitamin D supplementation than do lean individuals to achieve optimal levels of 25OHD 3 .Calcitriol modulates adipokine expression and inhibits anti-inflammatory cytokine expression. Calcitriol definitely has a role in the human adipose tissue because of its active form of vitamin D 3 metabolite, their receptors presented in adipocytes, and itse suppression of PTH levels.

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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 (PPARγ2)

Cited by 70 publications

References 21 publications

Pharmacological inhibition of PPARγ increases osteoblastogenesis and bone mass in male C57BL/6 mice

Pharmacological inhibition of PPARγ increases osteoblastogenesis and bone mass in male C57BL/6 mice

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Vitamin D and Obesity

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