Summary Objective To evaluate the quality of life (QoL) in patients with pituitary adenomas in comparison with healthy Mexican population QoL scores. Design & Measurements Cross‐sectional study using the short form 36 questionnaire (SF‐36) in 175 patients with pituitary adenomas grouped by adenoma subtype and disease activity, and compared them with the healthy Mexican population normative QoL scores. Patients A total of 44 patients with non‐functioning pituitary adenomas (NFPA), 48 with acromegaly, 53 with prolactinomas and 30 with Cushing disease (CD) were enrolled in this study. Results Mental and physical components scores (MCS & PCS) of SF‐36 questionnaire were lower in patients with active disease in all adenoma subtypes (P < 0.03). A significant negative relationship between prolactin levels and MCS (r = −0.30, P < 0.01) and PCS (r = −0.41, P < 0.01) were found in prolactinomas. Patients with CD showed 24 hours urine‐free cortisol levels negatively correlated with MCS (r = −0.43, P < 0.01) but not with PCS. No significant correlation was found between IGF‐1 ULN and QoL scores in acromegaly. NFPA patients had lower QoL scores than patients with controlled CD, acromegaly or prolactinoma (P < 0.02). Active CD and prolactinoma have lower QoL scores in comparison of NFPA (P < 0.05). Having an adenoma, secretory or non‐functioning, decrease QoL scores in comparison of results in the healthy Mexican population register. Using an adjusted‐multivariate model, we confirmed that disease activity in all secretory adenomas is an independent risk factor, reducing SF‐36 scores significantly. Conclusion Activity in all secretory pituitary adenomas’ patients decrease mental and physical QoL. However, independently of disease activity, secretory and NFPA significantly decrease QoL in comparison with healthy Mexican population QoL register.

Context & Objective Chronic glucocorticoid (GC) overexposure, resulting from endogenous Cushing’s syndrome (CS) or exogenous GC therapy, causes several adverse outcomes, including persistent central fat accumulation associated with a low-grade inflammation. However, no previous multi-omics studies in visceral adipose tissue (VAT) from patients exposed to high levels of unsuppressed GC during active CS or after remission are available yet. Methods We employed a translational approach combining high-throughput data on endogenous CS patients and a reversible CS mouse model. We performed RNA-seq and ChIP-seq on histone modifications (H3K4me3, H3K27ac and H3K27me3) to identify persistent transcriptional and epigenetic signatures in VAT produced during active CS and maintained after remission. Results VAT dysfunction was associated with low-grade pro-inflammatory status, macrophage infiltration and extracellular matrix remodeling. Most notably, chronic hypercortisolism caused a persistent circadian rhythm disruption in VAT through core clock genes modulation. Importantly, changes in the levels of two histone modifications associated to gene transcriptional activation (H3K4me3 and H3K27ac) correlated with the observed differences in gene expression during active CS and after CS remission. Conclusion We identified for the first time, the persistent transcriptional and epigenetic signatures induced by hypercortisolism in VAT, providing a novel integrated view of molecular components driving the long-term VAT impairment associated with CS.

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Development and severity of nonalcoholic fatty liver disease (NAFLD) have been linked to obesity and white adipose tissue (WAT) dysfunction plays a key role in this relation. We compared the main features of subcutaneous (SAT) and visceral WAT (VAT) tissue dysfunction in 48 obese women without (Ob) and with NAFLD (Ob-NAFLD) undergoing bariatric surgery and matched for age, BMI and T2D status. Fat cell area, adipocyte size distribution, the degree of histological fibrosis and the mRNA expression of adipokines and genes implicated in inflammation, adipogenesis, angiogenesis, metabolism and extracellular matrix remodeling were measured by RT-qPCR in both fat depots. Ob-NAFLD group showed higher TG and lower HDL circulating levels, increased VAT fat cell area and similar WAT fibrosis in comparison with Ob group. A sPLS-DA was performed in order to identify the set of genes that better characterize the presence of NAFLD. Finally, we build a multinomial logistic model including seven genes that explained 100% of the variance in NAFLD and correctly predicted 100% of cases. Our data support the existence of distinctive NAFLD signatures in WAT from women with severe obesity. A better understanding of these pathways may help in future strategies for the prevention and treatment of NAFLD.

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