Global 11 Beta-Hydroxysteroid Dehydrogenase Activity Assessed by the Circulating Cortisol to Cortisone Ratio is Associated with Features of Metabolic Syndrome

Serum cortisol-to-cortisone ratio and 11-deoxycortisol are associated with hypertension and blood pressure in Chinese rural population: a cross sectional study

“…Several previous epidemiological studies have assessed the relationships of F/E with hypertension and blood pressure. A study in Thailand found that the serum F/E was significantly higher in the hypertensive group than normotensive group, and regression analysis found a positive correlation between F/E and SBP, which was consistent with our findings, but no such association was found for DBP [22]. Another study of 350 Chilean children and adolescents with essential hypertension found that F/E was positively correlated with SBP and DBP [35].…”

“…F, the main form of GCs in the body, has been shown to be a reliable biomarker for HPA axis activity while E is a primary inactive metabolite of F [19][20][21]. Intriguingly, the cortisol-to-cortisone ratio (F/E) has been found that may serve as a proxy to global 11b-HSD activity [22]. Several studies have suggested potential clinical application of F/E assessment in the population with pulmonary hypertension or diabetes [23,24].…”

“…In addition, F is converted to non-MR bound cortisone facilitated by the 11b-HSD2 [12]. The administration of 11b-HSD2 inhibitors result in a change in the F/E, and MR was more likely to be activated by excess F, which causes hypertension [22,31]. Therefore, the mutual transformation of F and E may be tightly linked to hypertension.…”

“…Epidemiological studies have shown that higher F in adults with primary hypertension and in children with hypertension [21,32,33]. Furthermore, a few studies also suggested that serum F/E levels were associated with hypertension, but the association of F and E with blood pressure is inconsistent [22,31,[34][35][36][37]. S is converted to F mediated by CYP11B1.…”

Diagnóstico y tratamiento de la enfermedad de Cushing. Actualidades y posicionamiento del Grupo de Trabajo de Neuroendocrinología de la Sociedad Mexicana de Nutrición y Endocrinología

“…En el caso del HNN se ha propuesto que las condiciones que lo originan (alcoholismo, trastornos psiquiátricos) producen alteraciones en vías neuronales que finalmente estimulan a las neuronas del NPV para que incrementen la secreción de CRH o vasopresina, las cuales estimulan al corticotropo promoviendo la síntesis de ACTH, que finalmente actúa sobre receptores específicos de la corteza suprarrenal incrementando la síntesis y secreción de cortisol 2 . En el caso del síndrome metabólico, probablemente un incremento local en la actividad de la enzima 11β-hidroxiesteroide deshidrogenasa tipo 1 que convierte cortisona en cortisol sea el mayor responsable del HNN 2,4,5 .…”