Sansom Institute for Health Research, School of Pharmacy and Medical Sciences, University of South Australia, Adelaide, SA 5000, Australia.
Baker IDI Heart and Diabetes Institute, Melbourne, VIC 3004, Australia.
Nutrients. 2017 Aug 17;9(8):886. doi: 10.3390/nu9080886.
There is a body of evidence linking inflammation, altered lipid metabolism, and insulin resistance. Our previous research found that insulin sensitivity decreased after a four-week diet high in dairy compared to a control diet and to one high in red meat. Our aim was to determine whether a relationship exists between changes in insulin sensitivity and inflammatory biomarkers, or with lipid species. Fasting Tumor Necrosis Factor alpha (TNF-α), Tumor Necrosis Factor Receptor II (sTNF-RII), C-reactive protein (CRP), and lipids were measured at the end of each diet. TNF-α and the ratio TNF-α/sTNF-RII were not different between diets and TNF-α, sTNF-RII, or the ratio TNF-α/sTNF-RII showed no association with homeostasis model assessment-estimated insulin resistance (HOMA-IR). A number of phosphatidylethanolamine (PE) and phosphatidylinositol (PI) species differed between dairy and red meat and dairy and control diets, as did many phosphatidylcholine (PC) species and cholesteryl ester (CE) 14:0, CE15:0, lysophosphatidylcholine (LPC) 14:0, and LPC15:0. None had a significant relationship ( = 0.001 or better) with log homeostasis model assessment-estimated insulin resistance (HOMA-IR), although LPC14:0 had the strongest relationship ( = 0.004) and may be the main mediator of the effect of dairy on insulin sensitivity. LPC14:0 and the whole LPC class were correlated with CRP. The correlations between dietary change and the minor plasma phospholipids PI32:1 and PE32:1 are novel and may reflect significant changes in membrane composition. Inflammatory markers were not altered by changes in protein source while the correlation of LPC with CRP confirms a relationship between changes in lipid profile and inflammation.
有大量证据表明炎症、脂质代谢改变和胰岛素抵抗之间存在关联。我们之前的研究发现,与对照饮食和高红肉饮食相比,高乳制品饮食四周后胰岛素敏感性下降。我们的目的是确定胰岛素敏感性的变化与炎症生物标志物之间是否存在关系,或者与脂质种类是否存在关系。在每种饮食结束时测量空腹肿瘤坏死因子-α(TNF-α)、肿瘤坏死因子受体 II(sTNF-RII)、C 反应蛋白(CRP)和脂质。三种饮食之间 TNF-α 和 TNF-α/sTNF-RII 比值没有差异,且 TNF-α、sTNF-RII 或 TNF-α/sTNF-RII 比值与稳态模型评估估计的胰岛素抵抗(HOMA-IR)没有关联。在乳制品和红肉以及乳制品和对照饮食之间,有许多磷脂酰乙醇胺(PE)和磷脂酰肌醇(PI)种类以及许多磷脂酰胆碱(PC)种类和胆固醇酯(CE)14:0、CE15:0、溶血磷脂酰胆碱(LPC)14:0 和 LPC15:0 存在差异。虽然 LPC14:0 与 log HOMA-IR 具有最强的相关性(=0.004),并且可能是乳制品对胰岛素敏感性影响的主要介导物,但没有一种与 log HOMA-IR 具有显著相关性(=0.001 或更高)。LPC14:0 和整个 LPC 类与 CRP 相关。饮食变化与血浆磷脂 PI32:1 和 PE32:1 的微小变化之间的相关性是新颖的,可能反映了膜组成的显著变化。炎症标志物没有因蛋白质来源的变化而改变,而 LPC 与 CRP 的相关性证实了脂质谱变化与炎症之间的关系。