存在一种肥胖个体的表型,称为代谢健康肥胖,其呈现降低的心脏代谢风险。该表型为研究肥胖和代谢改变(例如2型糖尿病(T2DM))的连接机制提供了有价值的模型。以前,在一组病态肥胖女性的非目标代谢组学分析中,我们观察到代谢健康的病态肥胖个体和2型糖尿病相关个体的脂质代谢模式不同.为了验证这些发现,我们对脂质组学进行了补充研究.在这项研究中,我们对209名女性的血清样本进行了液相色谱和质谱联用的非靶向脂质组学分析。73名正常体重妇女(对照组)和136名病态肥胖妇女。从那些,65名代谢健康的病态肥胖和71名与T2DM相关。在这项工作中,我们发现神经酰胺水平升高,鞘磷脂,二酰基和三酰基甘油,脂肪酸,和磷酸乙醇胺在病态肥胖与正常体重之间的关系。相反,酰基肉碱水平下降,胆汁酸,溶血磷脂酰胆碱,磷脂酰胆碱(PC),磷脂酰肌醇,注意到和磷酸乙醇胺PE(O-38:4)。此外,比较患有T2DM的病态肥胖女性与代谢健康的MO,出现了独特的脂质分布,代谢产物水平增加:脱氧胆酸,二酰基甘油DG(36:2),三酰基甘油,磷脂酰胆碱,磷酸乙醇胺,磷脂酰肌醇,和溶血磷脂酰肌醇LPI(16:0)。最后,分析这两种比较,我们观察到脱氧胆酸水平下降,PC(34:3),病态肥胖女性与正常体重女性的PE(O-38:4)。相反,我们发现,与代谢健康的MO相比,患有T2DM的病态肥胖女性中这些脂质水平升高.这些代谢产物的特征可作为潜在的2型糖尿病在肥胖女性中代谢风险的标志物进行研究。
There is a phenotype of obese individuals termed metabolically healthy obese that present a reduced cardiometabolic risk. This phenotype offers a valuable model for investigating the mechanisms connecting obesity and metabolic alterations such as Type 2 Diabetes Mellitus (T2DM). Previously, in an untargeted metabolomics analysis in a cohort of morbidly obese women, we observed a different lipid metabolite pattern between metabolically healthy morbid obese individuals and those with associated T2DM. To validate these findings, we have performed a complementary
study of
lipidomics. In this
study, we assessed a liquid chromatography coupled to a mass spectrometer untargeted lipidomic analysis on serum samples from 209 women, 73 normal-weight women (control group) and 136 morbid obese women. From those, 65 metabolically healthy morbid obese and 71 with associated T2DM. In this work, we find elevated levels of ceramides, sphingomyelins, diacyl and triacylglycerols, fatty acids, and phosphoethanolamines in morbid obese vs normal weight. Conversely, decreased levels of acylcarnitines, bile acids, lyso-phosphatidylcholines, phosphatidylcholines (PC), phosphatidylinositols, and phosphoethanolamine PE (O-38:4) were noted. Furthermore, comparing morbid obese women with T2DM vs metabolically healthy MO, a distinct lipid profile emerged, featuring increased levels of metabolites: deoxycholic acid, diacylglycerol DG (36:2), triacylglycerols, phosphatidylcholines, phosphoethanolamines, phosphatidylinositols, and lyso-phosphatidylinositol LPI (16:0). To conclude, analysing both comparatives, we observed decreased levels of deoxycholic acid, PC (34:3), and PE (O-38:4) in morbid obese women vs normal-weight. Conversely, we found elevated levels of these lipids in morbid obese women with T2DM vs metabolically healthy MO. These profiles of metabolites could be explored for the research as potential markers of metabolic risk of T2DM in morbid obese women.