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首頁> 美國衛(wèi)生研究院文獻>ISRN Obesity >Downregulation of RelA (p65) by Rapamycin Inhibits Murine Adipocyte Differentiation and Reduces Fat Mass of C57BL/6J Mice despite High Fat Diet
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Downregulation of RelA (p65) by Rapamycin Inhibits Murine Adipocyte Differentiation and Reduces Fat Mass of C57BL/6J Mice despite High Fat Diet

機譯：雷帕霉素下調(diào)RelA（p65）抑制小鼠脂肪細胞分化并降低C57BL / 6J小鼠的脂肪量盡管高脂飲食

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Rapamycin (RAPA) is a clinical immunosuppressive agent first reported in the literature in 1975 after its discovery in a soil sample from the island of Rapa Nui. Aside from the well-documented effects of RAPA on cell division and immunologic response, the literature reveals it to have negative effects on adipocyte and osteocyte differentiation as well. Understanding of the molecular effects of RAPA on cell differentiation is fragmentary in regard to these cell lineages. In this paper, we examined a potential mechanism for RAPA's effects on adipocyte differentiation in vitro and in vivo. The data point to a unique role of Rel A (p65)—a component of the NF-κB system—in mediating this event. In murine adipose derived stem cell cultures (muADSCs) from C57BL/6J mice, RAPA was found to selectively downregulate RelA/p65, mammalian target of rapamycin (mTOR), and do so in a dose-dependent manner. This implies a novel role for RelA in adipocyte biology. Intracellular lipid accumulation—as subjectively observed—was also decreased in muADSCs treated with RAPA. Mice treated with RAPA had reduced overall body weight and reduced size of both intraabdominal and subcutaneous fat pads. When treated with RAPA, mice fed a high fat diet did not develop obesity and were not different from their regular diet controls in terms of body weight. These results suggested that RAPA inhibits adipogenesis and lipogenesis of muADSCs resulting in a prevention of obesity in C57BL/6J mice. This inhibition is strong enough to negate the effects of a high fat diet and seems to act by downregulating the RelA/p65 mTOR signaling pathway—a key component of the NF-κB family.
機譯：雷帕霉素（RAPA）是一種臨床免疫抑制劑，于1975年在Rapa Nui島的土壤樣本中發(fā)現(xiàn)后首次在文獻中報道。除了RAPA對細胞分裂和免疫反應的有據(jù)可查的影響外，文獻還顯示RAPA對脂肪細胞和骨細胞的分化也有不利影響。對于這些細胞譜系，了解RAPA對細胞分化的分子作用尚不完整。在本文中，我們研究了RAPA對體內(nèi)外脂肪細胞分化影響的潛在機制。數(shù)據(jù)表明，Rel A（p65）是NF-κB系統(tǒng)的組成部分，在介導此事件方面具有獨特作用。在來自C57BL / 6J小鼠的鼠類脂肪干細胞培養(yǎng)物中（muADSCs），發(fā)現(xiàn)RAPA選擇性下調(diào)雷帕霉素（mTOR）的哺乳動物靶標RelA / p65，并以劑量??依賴的方式進行。這暗示了RelA在脂肪細胞生物學中的新作用。如主觀觀察到的，在用RAPA處理的muADSC中，細胞內(nèi)脂質(zhì)的積累也減少了。用RAPA治療的小鼠體重減輕，腹部和皮下脂肪墊的尺寸減小。當用RAPA治療時，高脂飲食喂養(yǎng)的小鼠沒有出現(xiàn)肥胖癥，并且與常規(guī)飲食控制的體重沒有區(qū)別。這些結果表明，RAPA抑制muADSCs的脂肪生成和脂肪生成，從而預防了C57BL / 6J小鼠的肥胖。這種抑制作用足以抵消高脂飲食的影響，并且似乎通過下調(diào)RelA / p65 mTOR信號傳導途徑（NF-κB家族的關鍵組成部分）發(fā)揮作用。

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