Ginsenoside Rb1 promotes browning through regulation of PPARγ in 3T3-L1 adipocytes
Ginsenoside Rb1 promotes browning through regulation of PPARγ in 3T3-L1 adipocytes
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DOI：
10.1016/j.bbrc.2015.09.064
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发表时间：
2015-10-23
影响因子：
3.1
通讯作者：
Gao, Sihua
中科院分区：
文献类型：
--
作者：
Mu, Qianqian;Fang, Xin;Gao, Sihua
白色脂肪细胞组织（WAT）的布朗宁由于其在预防肥胖和相关合并症中的潜在意义而受到相当大的关注。据报道，人参皂苷Rb 1可改善肥胖动物的糖脂代谢并减轻体重。然而，体减少效应是否通过布朗宁效应介导尚不清楚。本研究以3 T3-L1脂肪细胞为研究对象，研究了人参皂甙Rb 1对布朗宁脂肪细胞特异性基因和耗氧量的影响。结果表明，10 μ M的Rb 1增加了基础葡萄糖摄取，并促进了布朗宁，这通过3 T3-L1成熟脂肪细胞中UCP-1、PGC-1 α和PRDM 16的mRNA表达的显著增加来证明。此外，Rb 1还增加了PPAR γ活性。而过氧化物酶体增殖物激活受体γ拮抗剂GW 9692则能消除这种布朗宁效应。此外，在3 T3-L1脂肪细胞中，TRb 1增加基础呼吸速率、ATP产生和解偶联能力。这些影响也被GW 9692减弱。结果表明，Rb 1通过诱导PPAR γ的表达促进3 T3-L1脂肪细胞的布朗宁。本研究结果为发现布朗宁激动剂提供了新的来源，也有助于了解和扩大人参及其成分的应用。(C)2015 Elsevier Inc. All rights reserved.
Browning of white adipocyte tissue (WAT) has received considerable attention due to its potential implication in preventing obesity and related comorbidities. Ginsenoside Rb1 is reported to improve glycolipid metabolism and reduce body weight in obese animals. However whether the body reducing effect mediates by browning effect remains unclear. For this purpose, 3T3-L1 adipocytes were used to study the effect of ginsenoside Rb1 on browning adipocytes specific genes and oxygen consumptions. The results demonstrate that 10 mu M of ginsenoside Rb1 increases basal glucose uptake and promoted browning evidenced by significant increases in mRNA expressions of UCP-1, PGC-1 alpha and PRDM16 in 3T3-L1 mature adipocytes. Further, ginsenoside Rb1 also increases PPAR gamma activity. And the browning effect is abrogated by GW9692, a PPAR gamma antagonist. In addition, ginsenoside Rb1 increases basal respiration rate, ATP production and uncoupling capacity in 3T3-L1 adipocytes. Those effects are also blunted by GW9692. The results suggest that ginsenoside Rb1 promote browning of 3T3-L1 adipocytes through induction of PPAR gamma. Our finding offer a new source to discover browning agonists and also useful to understand and extend the applications of ginseng and its constituents. (C) 2015 Elsevier Inc. All rights reserved.