近日，来自华盛顿州立大学的研究人员发现浆果、葡萄和其他水果能够将多余的白色脂肪转化为消耗卡路里的米色脂肪，这为肥胖的预防和治疗提供了新的策略。

　　在该项研究中，研究人员给小鼠饲喂了高脂饮食，并将小鼠分为两组，其中一组给予白藜芦醇处理，剂量相当于人类每天摄入12盎司的水果，一段时间后，给予白藜芦醇处理的高脂饮食小鼠其体重的增加比对照组小鼠少40%。

　　之前一些研究已经发现白藜芦醇能够帮助预防肥胖，但对其中的机制了解并不清楚。而且大部分相关研究都聚焦在葡萄酒上，所使用的白藜芦醇浓度也不能在正常饮食中获得。在该研究中，研究人员证明小鼠饮食中包含0.1%的白藜芦醇就能够将多余的白色脂肪转变为具有能量消耗活性的米色脂肪。研究人员解释道：水果中的多酚类物质，包括白藜芦醇，能够增加参与脂肪氧化过程的基因的表达，从而保证机体不会过载，这些多酚类物质能够促进白色脂肪组织转变为能够燃烧脂肪进行产热的米色脂肪，帮助机体保持能量平衡，从而预防肥胖和代谢紊乱的发生。

　　研究人员还发现调节机体能量代谢的重要分子AMPK在刺激白色脂肪向米色脂肪转变的过程中发挥了重要作用。

　　这项发表在国际学术期刊international journal of obesity上的研究对于肥胖的预防和治疗具有一定提示作用，多吃水果，有益代谢健康。

　　doi:10.1038/ijo.2015.23

　　Resveratrol induces brown-like adipocyte formation in white fat through activation of AMP-activated protein kinase (AMPK) α1

　　S Wang1,2,X Liang2,Q Yang2,X Fu2,C J Rogers2,M Zhu3,B D Rodgers2,Q Jiang1,M V Dodson2 and M Du

　　Objective:

　　Development of brown-like/beige adipocytes in white adipose tissue (WAT) helps to reduce obesity. Thus we investigated the effects of resveratrol, a dietary polyphenol capable of preventing obesity and related complications in humans and animal models, on brown-like adipocyte formation in inguinal WAT (iWAT).

　　Methods:

　　CD1 female mice (5-month old) were fed a high-fat diet with/without 0.1% resveratrol. In addition, primary stromal vascular cells separated from iWAT were subjected to resveratrol treatment. Markers of brown-like (beige) adipogenesis were measured and the involvement of AMP-activated protein kinase (AMPK) α1 was assessed using conditional knockout.

　　Results:

　　Resveratrol significantly increased mRNA and/or protein expression of brown adipocyte markers, including uncoupling protein 1 (UCP1), PR domain-containing 16, cell death-inducing DFFA-like effector A, elongation of very long-chain fatty acids protein 3, peroxisome proliferator-activated receptor-γ coactivator 1α, cytochrome c and pyruvate dehydrogenase, in differentiated iWAT stromal vascular cells (SVCs), suggesting that resveratrol induced brown-like adipocyte formation in vitro. Concomitantly, resveratrol markedly enhanced AMPKα1 phosphorylation and differentiated SVC oxygen consumption. Such changes were absent in cells lacking AMPKα1, showing that AMPKα1 is a critical mediator of resveratrol action. Resveratrol also induced beige adipogenesisin vivo along with the appearance of multiocular adipocytes, increased UCP1 expression and enhanced fatty acid oxidation.

　　Conclusions:

　　Resveratrol induces brown-like adipocyte formation in iWAT via AMPKα1 activation and suggest that its beneficial antiobesity effects may be partly due to the browning of WAT and, as a consequence, increased oxygen consumption.