Overexpression of superoxide dismutase 3 gene blocks high-fat diet-induced obesity, fatty liver and insulin resistance.
Overexpression of superoxide dismutase 3 gene blocks high-fat diet-induced obesity, fatty liver and insulin resistance.
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DOI：
10.1038/gt.2014.64
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发表时间：
2014-09
期刊：
影响因子：
5.1
通讯作者：
Liu, D.
中科院分区：
文献类型：
--
作者：
Cui, R.;Gao, M.;Qu, S.;Liu, D.
氧化应激在肥胖以及肥胖相关代谢紊乱的发展过程中起着重要作用。作为一种内源性抗氧化酶，超氧化物歧化酶3（SOD3）有可能影响饮食诱导的肥胖以及肥胖相关并发症。在当前的研究中，我们在喂食高脂肪饮食的C57BL/6小鼠中过表达SOD3，以研究其对高脂肪饮食诱导的肥胖、脂肪肝和胰岛素抵抗的影响。我们证明了Sod3基因转移阻止了高脂肪饮食诱导的肥胖、脂肪肝和胰岛素抵抗。对脂肪和肝脏组织的实时定量PCR分析显示，Sod3基因的过表达抑制了脂肪组织中促炎基因的表达，包括F4/80、TNFα、Cd11c、Mcp1和Il6，并增加了抗炎基因如脂联素的表达。在肝脏中，动物体内高水平的SOD3活性增强了负责能量消耗的基因的表达，包括Cpt1α、Cpt1β、Pgc1α、Pgc1β和Ucp2。这些结果表明，通过基因转移过表达Sod3基因是预防饮食诱导的肥胖以及肥胖相关并发症的一种有效方法。
Oxidative stress plays an important role in the development of obesity and obesity-associated metabolic disorders. As an endogenous antioxidant enzyme, superoxide dismutase 3 (SOD3) has the potential to affect diet-induced obesity and obesity associated complications. In the current work, we overexpressed SOD3 in C57BL/6 mice fed a high fat diet to study its effect on high fat diet-induced obesity, fatty liver and insulin resistance. We demonstrated that the Sod3 gene transfer blocked high fat diet induced obesity, fatty liver and insulin resistance. Real Time PCR analysis of adipose and liver tissues revealed that overexpression of the Sod3 gene suppressed expression of pro-inflammatory genes in adipose tissue including F4/80, Tnfα, Cd11c, Mcp1 and Il6, and increased expression of anti-inflammatory genes such as adiponectin. In the liver, high levels of SOD3 activity in animals enhanced expression of the genes responsible for energy expenditure including Cpt1α, Cpt1β, Pgc1α, Pgc1β and Ucp2. These results suggest that overexpression of the Sod3 gene through gene transfer is an effective approach in preventing diet induced obesity and obesity-associated complications.
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