Omega-3 fatty acids protect from diet-induced obesity, glucose intolerance, and adipose tissue inflammation through PPARγ-dependent and PPARγ-independent actions
Omega-3 fatty acids protect from diet-induced obesity, glucose intolerance, and adipose tissue inflammation through PPARγ-dependent and PPARγ-independent actions
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DOI：
10.1002/mnfr.201400914
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发表时间：
2015-05-01
影响因子：
5.2
通讯作者：
Festuccia, William
中科院分区：
文献类型：
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作者：
Belchior, Thiago;Paschoal, Vivian A.;Festuccia, William
适用范围：我们在此测试了过氧化物酶体增殖物激活受体γ（PPAR）是ω-3（n-3）对高脂饮食（HFD）诱导的肥胖、葡萄糖耐受不良和脂肪组织炎症的保护作用的主要介体的假设。给C57 BL 6野生型和fat-1转基因（fat-1）小鼠喂食低脂饮食（LFD）或HFD，用或不用PPAR γ拮抗剂处理，并评价能量平衡、肥胖、葡萄糖耐量和脂肪组织炎症。Fat-1小鼠免于肥胖、空腹高血糖、葡萄糖耐受不良和脂肪组织炎症。PPAR γ抑制完全消除了脂肪-1对HFD诱导的葡萄糖耐受不良的保护作用，但不包括肥胖或脂肪组织炎症。为了研究髓系细胞作为n-3代谢作用介质的作用，给髓系细胞中缺失（LyzM-PPAR γ（KO））或未缺失（LyzM-PPAR γ（WT））的小鼠喂食LFD或HFD（猪油）或富含n-3的HFD（鱼油）。结论：高水平的内源性n-3脂肪酸可减轻HFD引起的肥胖、糖耐量异常和脂肪组织炎症。其中，只有对葡萄糖耐受不良的保护作用是由非骨髓细胞的PPAR γ介导的。
Scope: We tested herein the hypothesis that peroxisome proliferator activated receptor gamma (PPAR) is a major mediator of omega-3 (n-3) protective actions against high-fat diet (HFD) induced obesity, glucose intolerance, and adipose tissue inflammation.Methods and results: C57BL6 wild-type and fat-1 transgenic (fat-1) mice were fed a low-fat diet (LFD) or HFD, treated or not with PPAR gamma antagonist, and evaluated for energy balance, adiposity, glucose tolerance, and adipose tissue inflammation. Fat-1 mice were protected from obesity, fasting hyperglycemia, glucose intolerance, and adipose tissue inflammation. PPAR gamma inhibition completely abolished fat-1 protection against HFD-induced glucose intolerance, but not obesity or adipose tissue inflammation. To investigate the role of myeloid cell as mediator of n-3 beneficialmetabolic actions, mice with deletion (LyzM-PPAR gamma(KO)) or nondeletion (LyzM-PPAR gamma(WT)) of PPAR gamma in myeloid cells were fed either LFD or HFD (lard) or an HFD rich in n-3 (fish oil). Our findings indicate that myeloid cell associated PPAR gamma is not involved in the attenuation of HFD-induced glucose intolerance and adipose tissue inflammation induced by n-3.Conclusion: High endogenous n-3 fatty acid levels protect from HFD obesity, glucose intolerance, and adipose tissue inflammation. Among these, only protection against glucose intolerance is mediated by non-myeloid cell PPAR gamma.