Triacylglycerol Fatty Acid Composition in Diet-Induced Weight Loss in Subjects with Abnormal Glucose Metabolism – the GENOBIN Study

BackgroundThe effect of weight loss on different plasma lipid subclasses at the molecular level is unknown. The aim of this study was to examine whether a diet-induced weight reduction result in changes in the extended plasma lipid profiles (lipidome) in subjects with features of metabolic syndrome in a 33-week intervention.
Methodology/Principal FindingsPlasma samples of 9 subjects in the weight reduction group and 10 subjects in the control group were analyzed using mass spectrometry based lipidomic and fatty acid analyses. Body weight decreased in the weight reduction group by 7.8±2.9% (p<0.01). Most of the serum triacylglycerols and phosphatidylcholines were reduced. The decrease in triacylglycerols affected predominantly the saturated short chain fatty acids. This decrease of saturated short chain fatty acid containing triacylglycerols correlated with the increase of insulin sensitivity. However, levels of several longer chain fatty acids, including arachidonic and docosahexanoic acid, were not affected by weight loss. Levels of other lipids known to be associated with obesity such as sphingolipids and lysophosphatidylcholines were not altered by weight reduction.
Conclusions/SignificanceDiet-induced weight loss caused significant changes in global lipid profiles in subjects with abnormal glucose metabolism. The observed changes may affect insulin sensitivity and glucose metabolism in these subjects.
Trial RegistrationClinicalTrials.gov NCT00621205

背景 目前尚不明确减重对不同血浆脂质亚类产生的分子层面影响。本研究旨在探究为期33周的干预试验中，饮食诱导的体重减轻是否会使携带代谢综合征特征的受试者的扩展型血浆脂质谱（脂质组，lipidome）发生改变。
方法学/主要研究结果 本研究采用基于质谱的脂质组学与脂肪酸分析方法，对减重组9名受试者与对照组10名受试者的血浆样本进行检测分析。减重组受试者的体重较基线下降7.8±2.9%（p<0.01）。多数血清三酰甘油与磷脂酰胆碱水平出现降低，其中三酰甘油的下降主要累及饱和短链脂肪酸酯化物；这类含饱和短链脂肪酸的三酰甘油水平下降与胰岛素敏感性升高呈显著相关。然而，包括花生四烯酸与二十二碳六烯酸在内的多种长链脂肪酸水平并未受减重干预影响。其余已知与肥胖相关的脂质，如鞘脂、溶血磷脂酰胆碱的水平亦未随体重减轻发生改变。
结论与意义 饮食诱导的减重可使糖代谢异常人群的整体脂质谱发生显著改变，上述观测到的变化或可影响此类人群的胰岛素敏感性与糖代谢过程。
试验注册 ClinicalTrials.gov NCT00621205