Group of Endocrine Disorders, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Carrer Rosselló, 149, 08036, Barcelona, Spain.
Endocrinology and Nutrition Department, Hospital Clínic, Barcelona, Spain.
J Mol Med (Berl). 2021 Aug;99(8):1085-1099. doi: 10.1007/s00109-021-02076-0. Epub 2021 Apr 21.
Chronic cortisol excess induces several alterations on protein, lipid and carbohydrate metabolism resembling those found in the metabolic syndrome. However, patients exposed to prolonged high levels of cortisol in Cushing syndrome (CS) present exceeding cardiometabolic alterations not reflected by conventional biomarkers. Using 3 ultra-high-performance liquid chromatography-tandem mass spectrometry (UHPLC-MS) platforms, we aimed to characterise the serum metabolome of 25 patients with active endogenous CS and 25 control subjects matched by propensity score (sex, BMI, diabetes mellitus type 2 (T2D), high blood pressure (HBP) and dyslipidaemia) to search for potential disease-specific biomarkers and pathways associated to the clinical comorbidities. A total of 93 metabolites were significantly altered in patients with CS. Increased levels of sulfur amino acids (AA), triacylglycerols, glycerophospholipids, ceramides and cholesteryl esters were observed. Contrarily, concentrations of essential and non-essential AA, polyunsaturated fatty acids, conjugated bile acids and second messenger glycerolipids were decreased. Twenty-four-hour urinary free cortisol (24h-UFC) independently determined the concentration of 21 lipids and 4 AA. A metabolic signature composed by 10 AA and 10 lipid metabolites presented an AUC-ROC of 95% for the classification of CS patients. Through differential network analysis, 152 aberrant associations between metabolites involved in the Lands cycle and Kennedy pathway were identified. Our data indicates that chronic hypercortisolemia confers a unique lipidomic signature and several alterations in numerous AA even when compared to patients with similar metabolic comorbidities providing novel insights of the increased cardiometabolic burden of CS. KEY MESSAGES: • Cortisol excess induces metabolic alterations beyond conventional biomarkers. • The hypercortisolism extent determines the concentration of 21 lipids and 5 aa. • Cortisol excess confers a unique metabolic signature of 20 metabolites. • Kennedy and Lands cycle are profoundly disturbed by cortisol excess.
慢性皮质醇过多会引起蛋白质、脂质和碳水化合物代谢的几种改变,类似于代谢综合征中发现的改变。然而,患有库欣综合征(CS)的患者长期暴露于高水平皮质醇会导致心血管代谢改变,而这些改变无法通过常规生物标志物反映出来。使用 3 种超高效液相色谱-串联质谱(UHPLC-MS)平台,我们旨在描述 25 例活动期内源性 CS 患者和 25 例按倾向评分(性别、BMI、2 型糖尿病(T2D)、高血压(HBP)和血脂异常)匹配的对照者的血清代谢组,以寻找潜在的与临床合并症相关的疾病特异性生物标志物和途径。CS 患者中有 93 种代谢物的水平显著改变。观察到含硫氨基酸(AA)、三酰甘油、甘油磷脂、神经酰胺和胆固醇酯水平升高。相反,必需和非必需 AA、多不饱和脂肪酸、结合胆汁酸和第二信使甘油脂质的浓度降低。24 小时尿游离皮质醇(24h-UFC)独立决定了 21 种脂质和 4 种 AA 的浓度。由 10 种 AA 和 10 种脂质代谢物组成的代谢特征对 CS 患者的分类具有 95%的 AUC-ROC。通过差异网络分析,确定了代谢物之间涉及 Lands 循环和 Kennedy 途径的 152 个异常关联。我们的数据表明,慢性皮质醇过多会导致独特的脂质组学特征和许多 AA 的改变,即使与具有相似代谢合并症的患者相比也是如此,这为 CS 增加的心血管代谢负担提供了新的见解。关键信息:
皮质醇过多会引起代谢改变,超出常规生物标志物的范围。
皮质醇过多的程度决定了 21 种脂质和 5 种 aa 的浓度。
皮质醇过多赋予了 20 种代谢物独特的代谢特征。
Kennedy 和 Lands 循环受到皮质醇过多的严重干扰。