Docosahexaenoic acid attenuates adipose tissue angiogenesis and insulin resistance in high fat diet-fed middle-aged mice via a sirt1-dependent mechanism
Docosahexaenoic acid attenuates adipose tissue angiogenesis and insulin resistance in high fat diet-fed middle-aged mice via a sirt1-dependent mechanism
复制标题
二十二碳六烯酸通过 Sirt1 依赖性机制减弱高脂肪饮食喂养的中年小鼠的脂肪组织血管生成和胰岛素抵抗。
DOI：
10.1002/mnfr.201500714
复制
发表时间：
2016-04-01
影响因子：
5.2
通讯作者：
Wang, Nanping
中科院分区：
文献类型：
--
作者：
Luo, Xiaoqin;Jia, Ru;Wang, Nanping
范围
二十二碳六烯酸（DHA; C22：6，n-3）是多不饱和脂肪酸（PUFA）的一种，对炎症性疾病、肥胖症和糖尿病具有有益作用。脂肪组织中的血管生成在肥胖及其相关代谢并发症的发展中具有重要作用。抑制血管生成是治疗肥胖的新策略。因此，我们研究了DHA对脂肪组织血管生成的影响，并研究了其潜在的机制。
方法和结果
在高脂饮食（HFD）喂养的中年小鼠中，DHA抑制脂肪组织中巨噬细胞源性炎症和血管生成，减少脂肪细胞大小和体脂组成，并改善胰岛素敏感性。此外，DHA逆转了HFD诱导的脂肪组织中Sirt 1的减少。有趣的是，DHA的作用被慢病毒介导的Sirt 1敲除减弱，同时巨噬细胞衍生的炎症和血管生成的标志物表达增加，与胰岛素敏感性受损相关。
结论
总的来说，我们的研究结果表明，DHA通过激活Sirt 1减少了脂肪组织的血管生成，并减弱了HFD诱导的肥胖小鼠的胰岛素抵抗。
SCOPE
Docosahexaenoic acid (DHA; C22: 6, n-3), one of PUFAs, exerts beneficial effects on inflammatory diseases, obesity and diabetes. Angiogenesis in adipose tissue has a major role in the development of obesity and its related metabolic complications. Inhibition of angiogenesis is an emerging strategy for the novel treatment for obesity. Thus, we examined the effect of DHA on angiogenesis in adipose tissues and investigated the underlying mechanisms.
METHODS AND RESULTS
In high-fat diet (HFD) fed middle-aged mice, DHA inhibited the macrophage-derived inflammation and angiogenesis in adipose tissues, reduced adipocyte size and body fat composition and improved insulin sensitivity. Moreover, DHA reversed the HFD-induced reduction of Sirt1 in adipose tissues. Interestingly, the effects of DHA were attenuated by lentivirus-mediated Sirt1 knockdown with increasing expression of markers of macrophage-derived inflammation and angiogenesis, associated with impaired insulin sensitivity.
CONCLUSION
Overall, our findings demonstrated that DHA reduced angiogenesis of adipose tissues and attenuated insulin resistance in HFD-induced obese mice via the activation of Sirt1.