Dietary saturated fatty acid type impacts obesity-induced metabolic dysfunction and plasma lipidomic signatures in mice.

Dietary saturated fatty acid type impacts obesity-induced metabolic dysfunction and plasma lipidomic signatures in mice.
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膳食饱和脂肪酸类型影响肥胖引起的代谢功能障碍和小鼠血浆脂质组学特征。

DOI:
10.1016/j.jnutbio.2018.10.005
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发表时间:
2019
期刊:
The Journal of nutritional biochemistry
影响因子:
--
通讯作者:
M. Picklo
M. Picklo
中科院分区:
--
文献类型:
--
作者:
P. Žáček;M. Bukowski;A. Mehus;L. Johnson;Huawei Zeng;S. Raatz;J. Idso;M. Picklo

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饱和脂肪酸(SFA)摄入与肥胖、胰岛素抵抗和肝脏脂肪变性有关,但很少有工作研究SFA类型对这些结果的影响。我们测试了这样一种假设:与增加长链SFA(LCSFA)(主要是棕榈酸)制备的肥胖饮食相比,由中链SFA(MCSFA)配制的肥胖饮食(主要是从椰子油中提取的月桂酸)可以减少肥胖诱导的结果。给16周的小鼠喂以对照组、低脂饲料或不同含量的MCSFA或LCSFA的肥胖饲料,其中多不饱和脂肪酸和单不饱和脂肪酸(PUFA;MUFA)保持不变。在肥胖饮食中加入MCSFA可防止肝脏脂肪堆积并降低胰岛素抵抗指数。肥胖饮食降低了肝脏新生血管生成蛋白(SCd1和Fasn)的水平,但提高了促炎症标志物Mcp-1和Tnfα的脂肪水平。血浆脂质组学分析表明,MCSFA摄入导致了与LCSFA摄入不同的血脂特征,阻止了促炎神经酰胺的升高,但某些脂质浓度的升高与心血管疾病风险增加有关。以SFA依赖的方式摄入肥胖饲料会增加含有长链多不饱和脂肪酸(LCPUFA)、花生四烯酸(ARA)和二十二碳六烯酸(DHA)的几种磷脂酰胆碱(PC)脂的血浆浓度,改变磷脂醚,并改变这些LCPUFA的三酰甘油环境。我们的数据表明,(1)MCSFA可降低某些肥胖共病的严重程度,(2)SFA类型调节与心血管疾病和糖尿病相关的脂类信号,(3)饮食SFA类型影响LCPUFA代谢。
Saturated fatty acid (SFA) intake is associated with obesity, insulin resistance, and hepatic steatosis, but scant work examines the impact of SFA type upon these outcomes. We tested the hypothesis that an obesogenic diet prepared with medium chain SFA (MCSFA), mostly as lauric acid-derived from coconut oil, reduces obesity-induced outcomes compared to obesogenic diets prepared with increasing amounts long chain SFA (LCSFA), primarily palmitic acid. Mice were fed (16 weeks) a control, low fat diet or obesogenic diets prepared with differing content of MCSFA or LCSFA in which polyunsaturated and monounsaturated fatty acids (PUFA; MUFA) were kept constant. Inclusion of MCSFA in an obesogenic diet prevented hepatic lipid accumulation and lowered indices of insulin resistance. Obesogenic diets reduced hepatic levels ofde novolipogenesis proteins (SCD1 and FASN) but elevated the adipose levels of mRNA for the pro-inflammatory markersMcp-1andTnfα. Lipidomic analysis of plasma indicated that MCSFA intake resulted in a different lipidomic signature than LCSFA intake, prevented elevation of pro-inflammatory ceramides, but elevated concentrations of some lipids associated with elevated cardiovascular disease risk. Intake of the obesogenic diets in an SFA-type dependent manner elevated plasma concentrations of several phosphatidylcholine (PC) lipids having the long chain PUFA (LCPUFA) arachidonic acid (ARA) and docosahexaenoic acid (DHA), altered phospholipid ethers, and changed the triacylglyceryl environments of these LCPUFA. Our data indicate that (1) MCSFA reduce the severity of some obesogenic co-morbidities, (2) SFA-type modulates lipidomic signatures associated with cardiovascular disease and diabetes, and (3) dietary SFA type impacts LCPUFA metabolism.
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