Lee Joseph J, Lambert Jennifer E, Hovhannisyan Yelena, Ramos-Roman Maria A, Trombold Justin R, Wagner David A, Parks Elizabeth J
From the Center for Human Nutrition, University of Texas Southwestern Medical Center, Dallas, TX (JJL, JEL, YH, and JRT); the Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX (MAR-R); Metabolic Solutions Inc., Nashua, NH (DAW); and the Department of Nutrition and Exercise Physiology, School of Medicine, University of Missouri, Columbia, MO (EJP).
Am J Clin Nutr. 2015 Jan;101(1):34-43. doi: 10.3945/ajcn.114.092262. Epub 2014 Nov 19.
Biochemical evidence has linked the coordinate control of fatty acid (FA) synthesis with the activity of stearoyl-CoA desaturase-1 (SCD1). The ratio of 16:1n-7 to 16:0 [SCD1₁₆] in plasma triacylglycerol FA has been used as an index to reflect liver SCD1₁₆ activity and has been proposed as a biomarker of FA synthesis, although this use has not been validated by comparison with isotopically measured de novo lipogenesis (DNL(Meas)).
We investigated plasma lipid 16:1n-7 and FA indexes of elongation and desaturation in relation to lipogenesis.
In this cross-sectional investigation of metabolism, 24 overweight adults, who were likely to have elevated DNL, consumed D2O for 10 d and had liver fat (LF) measured by magnetic resonance spectroscopy. Very-low-density lipoprotein (VLDL)-triacylglycerols and plasma free FA [nonesterified fatty acids (NEFAs)] were analyzed by using gas chromatography for the FA composition (molar percentage) and gas chromatography-mass spectrometry and gas chromatography-combustion isotope ratio mass spectrometry for deuterium enrichment.
In all subjects, VLDL-triacylglycerol 16:1n-7 was significantly (P < 0.01) related to DNL(Meas) (r = 0.56), liver fat (r = 0.53), and adipose insulin resistance (r = 0.56); similar positive relations were shown with the SCD1₁₆ index, and the pattern in NEFAs echoed that of VLDL-triacylglycerols. Compared with subjects with low LF (3.1 ± 2.7%; n = 11), subjects with high LF (18.4 ± 3.6%; n = 13) exhibited a 45% higher VLDL-triacylglycerol 16:1n-7 molar percentage (P < 0.01), 16% of subjects had lower 18:2n-6 (P = 0.01), and 27% of subjects had higher DNL as assessed by using a published DNL index (ratio of 16:0 to 18:2n-6; P = 0.03), which was isotopically confirmed by DNL(Meas) (increased 2.5-fold; P < 0.01). Compared with 16:0 in the diet, the low amount of dietary 16:1n-7 in VLDL-triacylglycerols corresponded to a stronger signal of elevated DNL.
The current data provide support for the use of the VLDL-triacylglycerol 16:1n-7 molar percentage as a biomarker for elevated liver fat when isotope use is not feasible; however, larger-scale confirmatory studies are needed.
生化证据表明脂肪酸（FA）合成的协同控制与硬脂酰辅酶A去饱和酶-1（SCD1）的活性有关。血浆三酰甘油FA中16:1n-7与16:0的比例[SCD1₁₆]已被用作反映肝脏SCD1₁₆活性的指标，并被提议作为FA合成的生物标志物，尽管这种用途尚未通过与同位素测量的从头脂肪生成（DNL(Meas)）进行比较来验证。
我们研究了血浆脂质16:1n-7以及伸长和去饱和的FA指标与脂肪生成的关系。
在这项代谢横断面研究中，24名超重成年人（可能具有升高的DNL）摄入重水10天，并通过磁共振波谱法测量肝脏脂肪（LF）。使用气相色谱法分析极低密度脂蛋白（VLDL）-三酰甘油和血浆游离FA[非酯化脂肪酸（NEFA）]的FA组成（摩尔百分比），并使用气相色谱-质谱联用仪和气相色谱-燃烧同位素比率质谱仪分析氘富集情况。
在所有受试者中，VLDL-三酰甘油16:1n-7与DNL(Meas)（r = 0.56）、肝脏脂肪（r = 0.53）和脂肪组织胰岛素抵抗（r = 0.56）显著相关（P < 0.01）；与SCD1₁₆指数也呈现相似的正相关关系，NEFA中的模式与VLDL-三酰甘油的模式相似。与低LF（3.1 ± 2.7%；n = 11）的受试者相比，高LF（18.4 ± 3.6%；n = 13）的受试者VLDL-三酰甘油16:1n-7摩尔百分比高45%（P < 0.01），16%的受试者18:2n-6较低（P = 0.01），27%的受试者使用已发表的DNL指数（16:0与18:2n-6的比率）评估时DNL较高（P = 0.03），这通过DNL(Meas)同位素证实（增加2.5倍；P < 0.01）。与饮食中的16:0相比，VLDL-三酰甘油中饮食16:1n-7含量较低对应着更强的DNL升高信号。
当前数据支持在无法使用同位素时，将VLDL-三酰甘油16:1n-7摩尔百分比用作肝脏脂肪升高的生物标志物；然而，需要更大规模的验证性研究。
