| Literature DB >> 33881561 |
Arturo Vega-Beyhart1,2, Marta Iruarrizaga3, Adriana Pané2, Guillermo García-Eguren1, Oriol Giró1, Laura Boswell1,2, Gloria Aranda1, Vanesa Flores1,2, Gregori Casals4, Cristina Alonso3, Mireia Mora1,2, Irene Halperin1,2, Francesc Carmona5, Joaquim Enseñat5, Oscar Vidal5, Ting Hu6, Gemma Rojo7,8, Ramon Gomis2,8,9,10, Felicia A Hanzu11,12,13,14.
Abstract
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.Entities:
Keywords: Biomarkers; Cortisol; Cushing syndrome; Lipidomics; Metabolomics
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Year: 2021 PMID: 33881561 DOI: 10.1007/s00109-021-02076-0
Source DB: PubMed Journal: J Mol Med (Berl) ISSN: 0946-2716 Impact factor: 4.599