Raspberry promotes brown and beige adipocyte development in mice fed high-fat diet through activation of AMP-activated protein kinase (AMPK) α1.
Raspberry promotes brown and beige adipocyte development in mice fed high-fat diet through activation of AMP-activated protein kinase (AMPK) α1.
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DOI：
10.1016/j.jnutbio.2018.02.005
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发表时间：
2018-05
期刊：
影响因子：
--
通讯作者：
Du M
中科院分区：
文献类型：
--
作者：
Zou T;Wang B;Yang Q;de Avila JM;Zhu MJ;You J;Chen D;Du M
棕色和米色/灰白色脂肪细胞的发育增加了产热作用，有助于减少肥胖和代谢综合征。我们之前的研究表明，饮食覆盆子可以改善饮食诱导的肥胖小鼠的代谢综合征。在这里，我们进一步评估了覆盆子对能量消耗和适应性产热的影响，并确定这些影响是否由amp活化蛋白激酶（AMPK）介导。将AMPKα1催化亚基缺失的小鼠和野生型（WT）小鼠分别饲喂高脂饮食（HFD）或添加5%覆盆子（RAS）的高脂饮食（HFD） 10周。评估脂肪组织的产热程序和相关调节因子。RAS改善了WT小鼠的胰岛素敏感性和脂肪量，而AMPKα1−/−小鼠则没有。在缺乏AMPKα1的情况下，RAS不能增加氧气消耗和产热。与此一致的是，在AMPKα1−/−小鼠中，RAS没有诱导棕色脂肪组织中产热基因的表达和皮下脂肪组织中棕色样脂肪细胞的形成。综上所述，AMPKα1在RAS影响褐色和米色/白白色脂肪细胞发育、预防肥胖和代谢功能障碍中不可或缺。
Development of brown and beige/brite adipocytes increases thermogenesis and helps to reduce obesity and metabolic syndrome. Our previous study suggests that dietary raspberry can ameliorate metabolic syndromes in diet-induced obese mice. Here, we further evaluated the effects of raspberry on energy expenditure and adaptive thermogenesis and determined whether these effects were mediated by AMP-activated protein kinase (AMPK). Mice deficient in the catalytic subunit of AMPKα1 and wild-type (WT) mice were fed a high-fat diet (HFD) or HFD supplemented with 5% raspberry (RAS) for 10 weeks. The thermogenic program and related regulatory factors in adipose tissue were assessed. RAS improved the insulin sensitivity and reduced fat mass in WT mice but not in AMPKα1−/− mice. In the absence of AMPKα1, RAS failed to increase oxygen consumption and heat production. Consistent with this, the thermogenic gene expression in brown adipose tissue and brown-like adipocyte formation in subcutaneous adipose tissue were not induced by RAS in AMPKα1−/− mice. In conclusion, AMPKα1 is indispensable for the effects of RAS on brown and beige/brite adipocyte development, and prevention of obesity and metabolic dysfunction.