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A high fat diet with a high C18:0/C16:0 ratio induced worse metabolic and transcriptomic profiles in C57BL/6 mice.
Lipids in Health and Disease ( IF 4.5 ) Pub Date : 2020-07-21 , DOI: 10.1186/s12944-020-01346-z
Liqiang Wang 1 , Fei Xu 1, 2 , Zhenfeng Song 3 , Dan Han 1 , Jingyi Zhang 1, 2 , Linjun Chen 1 , Lixin Na 1, 2, 3
Affiliation  

Differential effects of individual saturated fatty acids (SFAs), particularly stearic acid (C18:0), relative to the shorter-chain SFAs have drawn interest for more accurate nutritional guidelines. However, specific biologic and pathologic functions that can be assigned to particular SFAs are very limited. The present study was designed to compare changes in metabolic and transcriptomic profiles in mice caused by a high C18:0 diet and high palmitic acid (C16:0) diet. Male C57BL/6 mice were assigned to a normal fat diet (NFD), a high fat diet with high C18:0/C16:0 ratio (HSF) or an isocaloric high fat diet with a low C18:0/C16:0 ratio (LSF) for 10 weeks. An oral glucose tolerance test, 72-h energy expenditure measurement and CT scan of body fat were done before sacrifice. Fasting glucose and lipids were determined by an autobiochemical analyzer. Blood insulin, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) levels were measured by enzyme-linked immunosorbent assay methods. Free fatty acids (FFAs) profiles in blood and liver were determined by using gas chromatography-mass spectrometry. Microarray analysis was applied to investigate changes in transcriptomic profiles in the liver. Pathway analysis and gene ontology analysis were applied to describe the roles of differentially expressed mRNAs. Compared with the NFD group, body weight, body fat ratio, fasting blood glucose, insulin, homeostasis model assessment of insulin resistance (HOMA-IR), triglyceride, IL-6, serum and liver FFAs including total FFAs, C16:0 and C18:0 were increased in both high fat diet groups and were much higher in the HSF group than those in the LSF group. Both HSF and LSF mice exhibited distinguishable long non-coding RNA (lncRNA), microRNA and mRNA expression profiles when compared with those of NFD mice. Additionally, more differentially expressed lncRNAs and mRNAs were observed in the HSF group than in the LSF group. Some biological functions and pathways, other than energy metabolism regulation, were identified as differentially expressed mRNAs between the HSF group and the LSF group. The high fat diet with a high C18:0/C16:0 ratio induced more severe glucose and lipid metabolic disorders and inflammation and affected expression of more lncRNAs and mRNAs than an isocaloric low C18:0/C16:0 ratio diet in mice. These results provide new insights into the differences in biological functions and related mechanisms, other than glucose and lipid metabolism, between C16:0 and C18:0.

中文翻译:

具有高C18:0 / C16:0比的高脂饮食在C57BL / 6小鼠中引起较差的代谢和转录组学特征。

相对于短链SFA,单个饱和脂肪酸(SFA),特别是硬脂酸(C18:0)的差异作用引起了人们对更准确的营养指导方针的兴趣。但是,可以分配给特定SFA的特定生物学和病理功能非常有限。本研究旨在比较高C18:0饮食和高棕榈酸(C16:0)饮食引起的小鼠代谢和转录组谱变化。将雄性C57BL / 6小鼠指定为正常脂肪饮食(NFD),具有高C18:0 / C16:0比(HSF)的高脂肪饮食或具有低C18:0 / C16:0比的等热量高脂肪饮食(LSF)10周。处死前进行口服葡萄糖耐量试验,72小时能量消耗测量和体脂CT扫描。空腹血糖和脂质通过自动生化分析仪测定。通过酶联免疫吸附法测定血胰岛素,肿瘤坏死因子-α(TNF-α)和白介素-6(IL-6)的水平。使用气相色谱-质谱法测定血液和肝脏中的游离脂肪酸(FFA)谱。应用微阵列分析来研究肝脏中转录组谱的变化。应用途径分析和基因本体分析来描述差异表达的mRNA的作用。与NFD组相比,体重,体脂比,空腹血糖,胰岛素,胰岛素抵抗稳态模型评估(HOMA-IR),甘油三酸酯,IL-6,血清和肝脏FFA(包括总FFA,C16:0和C18)两种高脂饮食组中:0均升高,而HSF组中的LSF组中的:0更高。与NFD小鼠相比,HSF和LSF小鼠均表现出可区分的长非编码RNA(lncRNA),microRNA和mRNA表达谱。另外,在HSF组中观察到比LSF组中更多差异表达的lncRNA和mRNA。除能量代谢调节外,某些生物学功能和途径被鉴定为HSF组和LSF组之间差异表达的mRNA。与等热量的低C18:0 / C16:0比饮食相比,高C18:0 / C16:0比饮食高脂肪饮食诱导更严重的葡萄糖和脂质代谢紊乱和炎症,并影响更多的lncRNA和mRNA表达。这些结果为C16:0和C18:0之间除了葡萄糖和脂质代谢以外的生物学功能和相关机制的差异提供了新的见解。
更新日期:2020-07-21
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