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  1. Article: Hair cortisol and changes in cortisol dynamics in chronic kidney disease.

    Boswell, Laura / Vega-Beyhart, Arturo / Blasco, Miquel / Quintana, Luis F / Rodríguez, Gabriela / Díaz-Catalán, Daniela / Vilardell, Carme / Claro, María / Mora, Mireia / Amor, Antonio J / Casals, Gregori / Hanzu, Felicia A

    Frontiers in endocrinology

    2024  Volume 15, Page(s) 1282564

    Abstract: Objective: We compared hair cortisol (HC) with classic tests of the hypothalamic-pituitary-adrenal (HPA) axis in chronic kidney disease (CKD) and assessed its association with kidney and cardiometabolic status.: Design and methods: A cross-sectional ... ...

    Abstract Objective: We compared hair cortisol (HC) with classic tests of the hypothalamic-pituitary-adrenal (HPA) axis in chronic kidney disease (CKD) and assessed its association with kidney and cardiometabolic status.
    Design and methods: A cross-sectional study of 48 patients with CKD stages I-IV, matched by age, sex, and BMI with 24 healthy controls (CTR) was performed. Metabolic comorbidities, body composition, and HPA axis function were studied.
    Results: A total of 72 subjects (age 52.9 ± 12.2 years, 50% women, BMI 26.2 ± 4.1 kg/m
    Conclusion: Cortisol-after-DST and salivary cortisol rhythm present progressive alterations in CKD patients. Changes in cortisol excretion and HPA dynamics in CKD are not accompanied by significant changes in long-term exposure to cortisol evaluated by HC. The clinical significance and pathophysiological mechanisms explaining the associations between HPA parameters, body composition, and kidney damage warrant further study.
    MeSH term(s) Humans ; Cross-Sectional Studies ; Renal Insufficiency, Chronic/complications ; Renal Insufficiency, Chronic/drug therapy ; Hair/metabolism ; Hydrocortisone/metabolism ; Case-Control Studies ; Male ; Female ; Adult ; Middle Aged ; Aged ; Dexamethasone/therapeutic use ; Heart Disease Risk Factors ; Prospective Studies ; Hypothalamo-Hypophyseal System
    Chemical Substances Hydrocortisone (WI4X0X7BPJ) ; Dexamethasone (7S5I7G3JQL)
    Language English
    Publishing date 2024-03-25
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2592084-4
    ISSN 1664-2392
    ISSN 1664-2392
    DOI 10.3389/fendo.2024.1282564
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Ketoconazole- and Metyrapone-Induced Reductions on Urinary Steroid Metabolites Alter the Urinary Free Cortisol Immunoassay Reliability in Cushing Syndrome.

    Vega-Beyhart, Arturo / Laguna-Moreno, Javier / Díaz-Catalán, Daniela / Boswell, Laura / Mora, Mireia / Halperin, Irene / Casals, Gregori / Hanzu, Felicia A

    Frontiers in endocrinology

    2022  Volume 13, Page(s) 833644

    Abstract: Introduction: Twenty-four-hour urinary free cortisol (24h-UFC) is the most used test for follow-up decision-making in patients with Cushing syndrome (CS) under medical treatment. However, 24h-UFC determinations by immunoassays (IA) are commonly ... ...

    Abstract Introduction: Twenty-four-hour urinary free cortisol (24h-UFC) is the most used test for follow-up decision-making in patients with Cushing syndrome (CS) under medical treatment. However, 24h-UFC determinations by immunoassays (IA) are commonly overestimated because of steroid metabolites' cross-reaction. It is still uncertain how ketoconazole (KTZ)- and metyrapone (MTP)-induced changes on the urinary steroid metabolites can alter the 24h-UFC*IA determinations' reliability.
    Methods: 24h-UFC was analyzed by IA and gas chromatography-mass spectrometry (GC-MS) in 193 samples (81 before treatment, 73 during KTZ, and 39 during MTP) from 34 CS patients. In addition, urinary steroidome was analyzed by GC-MS on each patient before and during treatment.
    Results: Before treatment, 24h-UFC*IA determinations were overestimated by a factor of 1.75 (95% CI 1.60-1.94) compared to those by GC-MS. However, during KTZ treatment, 24h-UFC*IA results were similar (0.98:1) to those by GC-MS (95% CI, 0.83-1.20). In patients taking MTP, IA bias only decreased 0.55, resulting in persistence of an overestimation factor of 1.33:1 (95% CI, 1.09-1.76). High method agreement between GC-MS and IA before treatment (
    Conclusion: KTZ and MTP alter the urinary excretion of IA cross-reactive steroid metabolites, thus decreasing the cross-reactive interference of 24h-UFC*IA determinations present before treatment. Consequently, this interference reduction in 24h-UFC*IA leads to loss of method agreement with GC-MS and high risk of overestimating the biochemical impact of KTZ and MTP in controlling CS because of poor reliability of reference ranges and ULN.
    MeSH term(s) Cushing Syndrome/diagnosis ; Cushing Syndrome/drug therapy ; Humans ; Hydrocortisone/analysis ; Immunoassay ; Ketoconazole/therapeutic use ; Metyrapone ; Reproducibility of Results ; Steroids
    Chemical Substances Steroids ; Ketoconazole (R9400W927I) ; Hydrocortisone (WI4X0X7BPJ) ; Metyrapone (ZS9KD92H6V)
    Language English
    Publishing date 2022-02-23
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2592084-4
    ISSN 1664-2392
    ISSN 1664-2392
    DOI 10.3389/fendo.2022.833644
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Midnight Cortisol is Associated with Changes in Systolic Blood Pressure and Diabetic Neuropathy in Subjects with Type 1 Diabetes Undergoing Simultaneous Kidney-Pancreas Transplantation.

    Boswell, Laura / Amor, Antonio J / Montagud-Marrahi, Enrique / Casals, Gregori / Díaz-Catalan, Daniela / Banon-Maneus, Elisenda / Ramírez-Bajo, María José / Hierro, Natalia / Diekmann, Fritz / Musquera, Mireia / Serés-Noriega, Tonet / Esmatjes, Enric / Ferrer-Fàbrega, Joana / Ventura-Aguiar, Pedro / Hanzu, Felicia A

    Diabetes therapy : research, treatment and education of diabetes and related disorders

    2023  Volume 15, Issue 1, Page(s) 165–181

    Abstract: Introduction: An increased midnight cortisol (MC) has been described in end-stage kidney disease (ESKD) and type 1 diabetes (T1D). Lower circulating levels of the cytokine soluble tumor necrosis factor (TNF)-like weak inducer of apoptosis (sTWEAK) have ... ...

    Abstract Introduction: An increased midnight cortisol (MC) has been described in end-stage kidney disease (ESKD) and type 1 diabetes (T1D). Lower circulating levels of the cytokine soluble tumor necrosis factor (TNF)-like weak inducer of apoptosis (sTWEAK) have been found in T1D and ESKD and associated with cardiovascular (CV) events in the latter. We aimed to study MC and sTWEAK in simultaneous pancreas-kidney transplant (SPKT) recipients, and the association of these markers with CV risk factors and transplant outcomes.
    Methods: This was a retrospective cohort study including subjects with T1D who received a first SPKT between 2008 and 2020. MC and sTWEAK at baseline were correlated with CV risk factors and evolution 1 year after SPKT.
    Results: We included 29 subjects (58.6% women, mean age 43.5 ± 7.5 years, diabetes duration 31.9 ± 9.4 years). Systolic blood pressure (SBP) increased directly with MC quartiles, despite similar hypertension prevalence (p < 0.05). At 1 year, antihypertensive treatment was deintensified in those in lower MC quartiles (p < 0.05). Diabetic neuropathy prevalence decreased progressively in higher cortisol quartiles (p for trend = 0.005). Low MC was associated with delayed kidney graft function (p for trend = 0.044), and high sTWEAK with kidney graft rejection (p for trend = 0.018). In multivariate analyses, MC (standardized-β 0.505, p = 0.004) and age (standardized-β - 0.460, p = 0.040) were independently correlated with SBP, and MC was independently associated with the presence of diabetic neuropathy (OR 0.633, 95% CI 0.425-0.944, p = 0.025), adjusted for confounders.
    Conclusions: In this exploratory study, lower MC was associated with a lower baseline SBP, an improvement of antihypertensive treatment 1 year after transplant, and a higher diabetic neuropathy prevalence in SPKT recipients.
    Language English
    Publishing date 2023-11-02
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2566702-6
    ISSN 1869-6961 ; 1869-6953
    ISSN (online) 1869-6961
    ISSN 1869-6953
    DOI 10.1007/s13300-023-01487-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: BACE2 suppression in mice aggravates the adverse metabolic consequences of an obesogenic diet.

    Díaz-Catalán, Daniela / Alcarraz-Vizán, Gema / Castaño, Carlos / de Pablo, Sara / Rodríguez-Comas, Júlia / Fernández-Pérez, Antonio / Vallejo, Mario / Ramírez, Sara / Claret, Marc / Parrizas, Marcelina / Novials, Anna / Servitja, Joan-Marc

    Molecular metabolism

    2021  Volume 53, Page(s) 101251

    Abstract: Objective: Pancreatic β-cell dysfunction is a central feature in the pathogenesis of type 2 diabetes (T2D). Accumulating evidence indicates that β-site APP-cleaving enzyme 2 (BACE2) inhibition exerts a beneficial effect on β-cells in different models of ...

    Abstract Objective: Pancreatic β-cell dysfunction is a central feature in the pathogenesis of type 2 diabetes (T2D). Accumulating evidence indicates that β-site APP-cleaving enzyme 2 (BACE2) inhibition exerts a beneficial effect on β-cells in different models of T2D. Thus, targeting BACE2 may represent a potential therapeutic strategy for the treatment of this disease. Here, we aimed to investigate the effects of BACE2 suppression on glucose homeostasis in a model of diet-induced obesity.
    Methods: BACE2 knock-out (BKO) and wild-type (WT) mice were fed with a high-fat diet (HFD) for 2 or 16 weeks. Body weight, food intake, respiratory exchange ratio, locomotor activity, and energy expenditure were determined. Glucose homeostasis was evaluated by glucose and insulin tolerance tests. β-cell proliferation was assessed by Ki67-positive nuclei, and β-cell function was determined by measuring glucose-stimulated insulin secretion. Leptin sensitivity was evaluated by quantifying food intake and body weight after an intraperitoneal leptin injection. Neuropeptide gene expression and insulin signaling in the mediobasal hypothalamus were determined by qPCR and Akt phosphorylation, respectively.
    Results: After 16 weeks of HFD feeding, BKO mice exhibited an exacerbated body weight gain and hyperphagia, in comparison to WT littermates. Glucose tolerance was similar in both groups, whereas HFD-induced hyperinsulinemia, insulin resistance, and β-cell expansion were more pronounced in BKO mice. In turn, leptin-induced food intake inhibition and hypothalamic insulin signaling were impaired in BKO mice, regardless of the diet, in accordance with deregulation of the expression of hypothalamic neuropeptide genes. Importantly, BKO mice already showed increased β-cell proliferation and glucose-stimulated insulin secretion with respect to WT littermates after two weeks of HFD feeding, before the onset of obesity.
    Conclusions: Collectively, these results reveal that BACE2 suppression in an obesogenic setting leads to exacerbated body weight gain, hyperinsulinemia, and insulin resistance. Thus, we conclude that inhibition of BACE2 may aggravate the adverse metabolic effects associated with obesity.
    MeSH term(s) Amyloid Precursor Protein Secretases/metabolism ; Animals ; Aspartic Acid Endopeptidases/metabolism ; Diet/adverse effects ; Male ; Mice ; Mice, Transgenic ; Obesity/metabolism
    Chemical Substances Bace2 protein, mouse ; Amyloid Precursor Protein Secretases (EC 3.4.-) ; Aspartic Acid Endopeptidases (EC 3.4.23.-)
    Language English
    Publishing date 2021-05-17
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2708735-9
    ISSN 2212-8778 ; 2212-8778
    ISSN (online) 2212-8778
    ISSN 2212-8778
    DOI 10.1016/j.molmet.2021.101251
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: 4-Phenylbutyrate (PBA) treatment reduces hyperglycemia and islet amyloid in a mouse model of type 2 diabetes and obesity.

    de Pablo, Sara / Rodríguez-Comas, Júlia / Díaz-Catalán, Daniela / Alcarraz-Vizán, Gema / Castaño, Carlos / Moreno-Vedia, Juan / Montane, Joel / Parrizas, Marcelina / Servitja, Joan-Marc / Novials, Anna

    Scientific reports

    2021  Volume 11, Issue 1, Page(s) 11878

    Abstract: Amyloid deposits in pancreatic islets, mainly formed by human islet amyloid polypeptide (hIAPP) aggregation, have been associated with loss of β-cell mass and function, and are a pathological hallmark of type 2 diabetes (T2D). Treatment with chaperones ... ...

    Abstract Amyloid deposits in pancreatic islets, mainly formed by human islet amyloid polypeptide (hIAPP) aggregation, have been associated with loss of β-cell mass and function, and are a pathological hallmark of type 2 diabetes (T2D). Treatment with chaperones has been associated with a decrease in endoplasmic reticulum stress leading to improved glucose metabolism. The aim of this work was to investigate whether the chemical chaperone 4-phenylbutyrate (PBA) prevents glucose metabolism abnormalities and amyloid deposition in obese agouti viable yellow (A
    MeSH term(s) Amyloid/metabolism ; Animals ; Diabetes Mellitus, Experimental/drug therapy ; Diabetes Mellitus, Experimental/metabolism ; Diabetes Mellitus, Type 2/drug therapy ; Diabetes Mellitus, Type 2/metabolism ; Disease Models, Animal ; Female ; Glucose Intolerance/metabolism ; Glucose Tolerance Test ; Homeostasis ; Hyperglycemia/drug therapy ; Hyperglycemia/metabolism ; Insulin Secretion ; Insulin-Secreting Cells/metabolism ; Islet Amyloid Polypeptide/metabolism ; Islets of Langerhans/metabolism ; Male ; Mice ; Mice, Transgenic ; Obesity/drug therapy ; Obesity/metabolism ; Phenylbutyrates/pharmacology
    Chemical Substances Amyloid ; Islet Amyloid Polypeptide ; Phenylbutyrates ; 4-phenylbutyric acid (7WY7YBI87E)
    Language English
    Publishing date 2021-06-04
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-021-91311-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Alpha1-antitrypsin ameliorates islet amyloid-induced glucose intolerance and β-cell dysfunction.

    Rodríguez-Comas, Júlia / Moreno-Vedia, Juan / Obach, Mercè / Castaño, Carlos / de Pablo, Sara / Alcarraz-Vizán, Gema / Díaz-Catalán, Daniela / Mestre, Anna / Horrillo, Raquel / Costa, Montserrat / Novials, Anna / Servitja, Joan-Marc

    Molecular metabolism

    2020  Volume 37, Page(s) 100984

    Abstract: Objective: Pancreatic β-cell failure is central to the development and progression of type 2 diabetes (T2D). The aggregation of human islet amyloid polypeptide (hIAPP) has been associated with pancreatic islet inflammation and dysfunction in T2D. Alpha1- ...

    Abstract Objective: Pancreatic β-cell failure is central to the development and progression of type 2 diabetes (T2D). The aggregation of human islet amyloid polypeptide (hIAPP) has been associated with pancreatic islet inflammation and dysfunction in T2D. Alpha1-antitrypsin (AAT) is a circulating protease inhibitor with anti-inflammatory properties. Here, we sought to investigate the potential therapeutic effect of AAT treatment in a mouse model characterized by hIAPP overexpression in pancreatic β-cells.
    Methods: Mice overexpressing hIAPP (hIAPP-Tg) in pancreatic β-cells were used as a model of amyloid-induced β-cell dysfunction. Glucose homeostasis was evaluated by glucose tolerance tests and insulin secretion assays. Apoptosis and amyloid formation was assessed in hIAPP-Tg mouse islets cultured at high glucose levels. Dissociated islet cells were cocultured with macrophages obtained from the peritoneal cavity.
    Results: Nontreated hIAPP-Tg mice were glucose intolerant and exhibited impaired insulin secretion. Interestingly, AAT treatment improved glucose tolerance and restored the insulin secretory response to glucose in hIAPP-Tg mice. Moreover, AAT administration normalized the expression of the essential β-cell genes MafA and Pdx1, which were downregulated in pancreatic islets from hIAPP-Tg mice. AAT prevented the formation of amyloid deposits and apoptosis in hIAPP-Tg islets cultured at high glucose concentrations. Since islet macrophages mediate hIAPP-induced β-cell dysfunction, we investigated the effect of AAT in cocultures of macrophages and islet cells. AAT prevented hIAPP-induced β-cell apoptosis in these cocultures without reducing the hIAPP-induced secretion of IL-1β by macrophages. Remarkably, AAT protected β-cells against the cytotoxic effects of conditioned medium from hIAPP-treated macrophages. Similarly, AAT also abrogated the cytotoxic effects of exogenous proinflammatory cytokines on pancreatic β-cells.
    Conclusions: These results demonstrate that treatment with AAT improves glucose homeostasis in mice overexpressing hIAPP and protects pancreatic β-cells from the cytotoxic actions of hIAPP mediated by macrophages. These results support the use of AAT-based therapies to recover pancreatic β-cell function for the treatment of T2D.
    MeSH term(s) Amyloid/metabolism ; Animals ; Apoptosis ; Blood Glucose/metabolism ; Diabetes Mellitus, Type 2/metabolism ; Disease Models, Animal ; Glucose/metabolism ; Glucose Intolerance/metabolism ; Glucose Tolerance Test ; Humans ; Insulin/metabolism ; Insulin Secretion ; Insulin-Secreting Cells/metabolism ; Insulin-Secreting Cells/physiology ; Islet Amyloid Polypeptide/genetics ; Islet Amyloid Polypeptide/metabolism ; Islets of Langerhans/metabolism ; Islets of Langerhans/physiology ; Macrophages/metabolism ; Male ; Mice ; Mice, Transgenic ; alpha 1-Antitrypsin/genetics ; alpha 1-Antitrypsin/metabolism
    Chemical Substances Amyloid ; Blood Glucose ; Insulin ; Islet Amyloid Polypeptide ; alpha 1-Antitrypsin ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2020-03-27
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2708735-9
    ISSN 2212-8778 ; 2212-8778
    ISSN (online) 2212-8778
    ISSN 2212-8778
    DOI 10.1016/j.molmet.2020.100984
    Database MEDical Literature Analysis and Retrieval System OnLINE

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