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Dive into the research topics where Cidália Dionísio Pereira is active.

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Featured researches published by Cidália Dionísio Pereira.


Endoscopy | 2012

Management of precancerous conditions and lesions in the stomach (MAPS): guideline from the European Society of Gastrointestinal Endoscopy (ESGE), European Helicobacter Study Group (EHSG), European Society of Pathology (ESP), and the Sociedade Portuguesa de Endoscopia Digestiva (SPED)

Mário Dinis-Ribeiro; Miguel Areia; A. C. de Vries; Ricardo Marcos-Pinto; M. Monteiro-Soares; A. O’Connor; Cidália Dionísio Pereira; Pedro Pimentel-Nunes; Rui Correia; Arzu Ensari; Jean-Marc Dumonceau; José Carlos Machado; Guilherme Macedo; Peter Malfertheiner; Tamara Matysiak-Budnik; Francis Mégraud; K. Miki; Colm O’Morain; Richard M. Peek; Thierry Ponchon; Ari Ristimäki; B. Rembacken; Fátima Carneiro; E. J. Kuipers

Atrophic gastritis, intestinal metaplasia, and epithelial dysplasia of the stomach are common and are associated with an increased risk for gastric cancer. In the absence of guidelines, there is wide disparity in the management of patients with these premalignant conditions. The European Society of Gastrointestinal Endoscopy (ESGE), the European Helicobacter Study Group (EHSG), the European Society of Pathology (ESP) and the Sociedade Portuguesa de Endoscopia Digestiva (SPED) have therefore combined efforts to develop evidence-based guidelines on the management of patients with precancerous conditions and lesions of the stomach (termed MAPS). A multidisciplinary group of 63 experts from 24 countries developed these recommendations by means of repeat online voting and a meeting in June 2011 in Porto, Portugal. The recommendations emphasize the increased cancer risk in patients with gastric atrophy and metaplasia, and the need for adequate staging in the case of high grade dysplasia, and they focus on treatment and surveillance indications and methods.


Diabetes, Obesity and Metabolism | 2012

11β-Hydroxysteroid dehydrogenase type 1: relevance of its modulation in the pathophysiology of obesity, the metabolic syndrome and type 2 diabetes mellitus.

Cidália Dionísio Pereira; Isabel Azevedo; Rosário Monteiro; Maria João Martins

Recent evidence strongly argues for a pathogenic role of glucocorticoids and 11β‐hydroxysteroid dehydrogenase type 1 (11β‐HSD1) in obesity and the metabolic syndrome, a cluster of risk factors for atherosclerotic cardiovascular disease and type 2 diabetes mellitus (T2DM) that includes insulin resistance (IR), dyslipidaemia, hypertension and visceral obesity. This has been partially prompted not only by the striking clinical resemblances between the metabolic syndrome and Cushings syndrome (a state characterized by hypercortisolism that associates with metabolic syndrome components) but also from monogenic rodent models for the metabolic syndrome (e.g. the leptin‐deficient ob/ob mouse or the leptin‐resistant Zucker rat) that display overall increased secretion of glucocorticoids. However, systemic circulating glucocorticoids are not elevated in obese patients and/or patients with metabolic syndrome. The study of the role of 11β‐HSD system shed light on this conundrum, showing that local glucocorticoids are finely regulated in a tissue‐specific manner at the pre‐receptor level. The system comprises two microsomal enzymes that either activate cortisone to cortisol (11β‐HSD1) or inactivate cortisol to cortisone (11β‐HSD2). Transgenic rodent models, knockout (KO) for HSD11B1 or with HSD11B1 or HSD11B2 overexpression, specifically targeted to the liver or adipose tissue, have been developed and helped unravel the currently undisputable role of the enzymes in metabolic syndrome pathophysiology, in each of its isolated components and in their prevention. In the transgenic HSD11B1 overexpressing models, different features of the metabolic syndrome and obesity are replicated. HSD11B1 gene deficiency or HSD11B2 gene overexpression associates with improvements in the metabolic profile. In face of these demonstrations, research efforts are now being turned both into the inhibition of 11β‐HSD1 as a possible pharmacological target and into the role of dietary habits on the establishment or the prevention of the metabolic syndrome, obesity and T2DM through 11β‐HSD1 modulation. We intend to review and discuss 11β‐HSD1 and obesity, the metabolic syndrome and T2DM and to highlight the potential of its inhibition for therapeutic or prophylactic approaches in those metabolic diseases.


International Journal of Endocrinology | 2014

Relevance of a Hypersaline Sodium-Rich Naturally Sparkling Mineral Water to the Protection against Metabolic Syndrome Induction in Fructose-Fed Sprague-Dawley Rats: A Biochemical, Metabolic, and Redox Approach

Cidália Dionísio Pereira; Milton Severo; João R. Araújo; João Tiago Guimarães; Diogo Pestana; Alejandro Santos; Rita Ferreira; António Ascensão; José Magalhães; Isabel Azevedo; Rosário Monteiro; Maria João Martins

The Metabolic Syndrome increases the risk for atherosclerotic cardiovascular disease and type 2 Diabetes Mellitus. Increased fructose consumption and/or mineral deficiency have been associated with Metabolic Syndrome development. This study aimed to investigate the effects of 8 weeks consumption of a hypersaline sodium-rich naturally sparkling mineral water on 10% fructose-fed Sprague-Dawley rats (Metabolic Syndrome animal model). The ingestion of the mineral water (rich in sodium bicarbonate and with higher potassium, calcium, and magnesium content than the tap water used as control) reduced/prevented not only the fructose-induced increase of heart rate, plasma triacylglycerols, insulin and leptin levels, hepatic catalase activity, and organ weight to body weight ratios (for liver and both kidneys) but also the decrease of hepatic glutathione peroxidase activity and oxidized glutathione content. This mineral-rich water seems to have potential to prevent Metabolic Syndrome induction by fructose. We hypothesize that its regular intake in the context of modern diets, which have a general acidic character interfering with mineral homeostasis and are poor in micronutrients, namely potassium, calcium, and magnesium, could add surplus value and attenuate imbalances, thus contributing to metabolic and redox health and, consequently, decreasing the risk for atherosclerotic cardiovascular disease.


Asian Journal of Andrology | 2014

Effects of natural mineral-rich water consumption on the expression of sirtuin 1 and angiogenic factors in the erectile tissue of rats with fructose-induced metabolic syndrome

Cidália Dionísio Pereira; Milton Severo; Luísa Rafael; Maria João Martins; Delminda Neves

Consuming a high-fructose diet induces metabolic syndrome (MS)-like features, including endothelial dysfunction. Erectile dysfunction is an early manifestation of endothelial dysfunction and systemic vascular disease. Because mineral deficiency intensifies the deleterious effects of fructose consumption and mineral ingestion is protective against MS, we aimed to characterize the effects of 8 weeks of natural mineral-rich water consumption on the structural organization and expression of vascular growth factors and receptors on the corpus cavernosum (CC) in 10% fructose-fed Sprague-Dawley rats (FRUCT). Differences were not observed in the organization of the CC either on the expression of vascular endothelial growth factor (VEGF) or the components of the angiopoietins/Tie2 system. However, opposing expression patterns were observed for VEGF receptors (an increase and a decrease for VEGFR1 and VEGFR2, respectively) in FRUCT animals, with these patterns being strengthened by mineral-rich water ingestion. Mineral-rich water ingestion (FRUCTMIN) increased the proportion of smooth muscle cells compared with FRUCT rats and induced an upregulatory tendency of sirtuin 1 expression compared with the control and FRUCT groups. Western blot results were consistent with the dual immunofluorescence evaluation. Plasma oxidized low-density lipoprotein and plasma testosterone levels were similar among the experimental groups, although a tendency for an increase in the former was observed in the FRUCTMIN group. The mineral-rich water-treated rats presented changes similar to those observed in rats treated with MS-protective polyphenol-rich beverages or subjected to energy restriction, which led us to hypothesize that the effects of mineral-rich water consumption may be more vast than those directly observed in this study.


Life Sciences | 2015

Role of physical exercise on hepatic insulin, glucocorticoid and inflammatory signaling pathways in an animal model of non-alcoholic steatohepatitis

Emanuel Passos; Cidália Dionísio Pereira; Inês O. Gonçalves; Sílvia Rocha-Rodrigues; Nuno Silva; João Tiago Guimarães; Delminda Neves; António Ascensão; José Magalhães; Maria João Martins

AIMS Pro-inflammatory mediators, glucocorticoids and transforming growth factor (TGF)-β are implicated in the pathogenesis of non-alcoholic steatohepatitis (NASH)-related insulin resistance. As physical activity is beneficial against NASH, we analyzed the voluntary physical activity (VPA) and endurance training (ET) (preventive and therapeutic strategies) effects on hepatic insulin, pro-inflammatory and glucocorticoid signaling regulators/mediators in high-fat (Lieber-DeCarli) diet (HFD)-induced NASH. MAIN METHODS Adult male Sprague-Dawley rats were divided in standard diet (SD) or HFD, with sedentary, VPA and ET animals in both diet regimens. Plasma glucose and insulin concentrations were analyzed; plasma insulin sensitivity index (ISI) was calculated. Hepatic insulin, pro-inflammatory and glucocorticoid signaling regulators/mediators were evaluated by Western blot or reverse transcriptase-PCR. KEY FINDINGS ET improved ISI in both diet regimens. HFD-feeding increased interleukin-1β and induced a similar pattern on interleukin-6 and TGF-β, which were globally reduced by physical exercise. ET decreased HFD leukemia inhibitory factor level, SD+VPA animals presenting higher values than HFD+VPA animals. HFD increased the ratio of IRS-1(Ser307)/total IRS-1, which was completely mitigated by physical exercise. Physical exercise reduced total ERK and JNK (total and activated) expression in HFD. In SD vs. HFD, VPA presented higher activated JNK and ET presented higher total JNK. Generally, in HFD, the ratio (activated/total) of AKT, and each separately, decreased with exercise and also for activated AKT in SD. Overall, in both diets, exercise reduced 11β-hydroxysteroid dehydrogenase type 1. ET increased glucocorticoid receptor and reduced PTP1B in HFD. SIGNIFICANCE Physical exercise mitigates the expression of pro-inflammatory mediators and positively modulates insulin and glucocorticoid signaling in NASH.


Hormone Molecular Biology and Clinical Investigation | 2015

Natural mineral-rich water ingestion improves hepatic and fat glucocorticoid-signaling and increases sirtuin 1 in an animal model of metabolic syndrome

Cidália Dionísio Pereira; Milton Severo; Delminda Neves; António Ascensão; José Magalhães; João Tiago Guimarães; Rosário Monteiro; Maria João Martins

Abstract Background: We recently reported protection against metabolic syndrome (MetSyn) induction and endothelial dysfunction by natural mineral-rich water intake in fructose-fed Sprague-Dawley rats. As glucocorticoids are critical to MetSyn development, we aimed to further characterize the beneficial effects of mineral-rich water intake in that animal model, by assessing relevant effectors in glucocorticoid-signaling in liver and subcutaneous (SCAT) and visceral (VAT) adipose tissues, sites with a central role in metabolic (dys)regulation. Materials and methods: Adult male rats had free access to standard diet and different drinking solutions (8 weeks): a) tap water (CONT), b) 10% fructose/tap water (FRUCT) or c) 10% fructose/mineral-rich water (FRUCTMIN). 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), glucocorticoid receptor (GR), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1-α) and sirtuin 1 (Sirt1) tissue protein expressions were evaluated by Western blot. Plasma corticosterone (ELISA) and non-esterified fatty acids (NEFA) levels were quantified spectrophotometrically. Results: Expectedly, Sirt1 and PGC1-α significantly decreased in liver, 11β-HSD1 tended to increase in VAT and tended to decrease in liver and SCAT, and plasma corticosterone tended to increase in FRUCT vs. CONT. Mineral-rich water showed a trend towards a reduction of these fructose effects and significantly increased hepatic Sirt1 vs. CONT and FRUCT. GR significantly increased in VAT and plasma NEFA strongly tended to increase in FRUCTMIN vs. CONT and FRUCT. Conclusions: Glucocorticoid-signaling was different among SCAT and VAT and also in liver. Mineral-rich water modulation of fructose effects on glucocorticoid-signaling and Sirt1 underlines the better metabolic profile found earlier.


Hormone Molecular Biology and Clinical Investigation | 2016

Ingestion of a natural mineral-rich water in an animal model of metabolic syndrome: effects in insulin signalling and endoplasmic reticulum stress

Cidália Dionísio Pereira; Emanuel Passos; Milton Severo; Isabel Vitó; Xiaogang Wen; Fátima Carneiro; Pedro Gomes; Rosário Monteiro; Maria João Martins

Abstract Background: High-fructose and/or low-mineral diets are relevant in metabolic syndrome (MS) development. Insulin resistance (IR) represents a central mechanism in MS development. Glucocorticoid signalling dysfunction and endoplasmic reticulum (ER) and oxidative stresses strongly contribute to IR and associate with MS. We have described that natural mineral-rich water ingestion delays fructose-induced MS development, modulates fructose effects on the redox state and glucocorticoid signalling and increases sirtuin 1 expression. Here, we investigated mineral-rich water ingestion effects on insulin signalling and ER homeostasis of fructose-fed rats. Materials and methods: Adult male Sprague-Dawley rats had free access to standard-chow diet and different drinking solutions (8 weeks): tap water (CONT), 10%-fructose/tap water (FRUCT) or 10%-fructose/mineral-rich water (FRUCTMIN). Hepatic and adipose (visceral, VAT) insulin signalling and hepatic ER homeostasis (Western blot or PCR) as well as hepatic lipid accumulation were evaluated. Results: Hepatic p-IRS1Ser307/IRS1 (tendency), p-IRS1Ser307, total JNK and (activated IRE1α)/(activated JNK) decreased with fructose ingestion, while p-JNK tended to increase; mineral-rich water ingestion, totally or partially, reverted all these effects. Total PERK, p-eIF2α (tendency) and total IRS1 (tendency) decreased in both fructose-fed groups. p-ERK/ERK and total IRE1α increasing tendencies in FRUCT became significant in FRUCTMIN (similar pattern for lipid area). Additionally, unspliced-XBP1 increased with mineral-rich water. In VAT, total ERK fructose-induced increase was partially prevented in FRUCTMIN. Conclusions: Mineral-rich water modulation of fructose-induced effects on insulin signalling and ER homeostasis matches the better metabolic profile previously reported. Increased p-ERK/ERK, adding to decreased IRE1α activation, and increased unspliced-XBP1 and lipid area may protect against oxidative stress and IR development in FRUCTMIN.


Archive | 2012

11β-Hydroxysteroid Dehydrogenases in the Regulation of Tissue Glucocorticoid Availability

Cidália Dionísio Pereira; Rosário Monteiro; Miguel Constância; Maria João Martins

The regulation of tissue-specific actions of glucocorticoids (GCs) goes far beyond the effects of the fluctuation of their circulating levels and can be controlled by local intracellular en‐ zymes. In the past few years, evidence is being gathered not only on the relevance of such enzymes to GC physiological actions but also on their involvement in the pathophysiology of certain chronic disease states, in which circulating GC levels are not necessarily altered. These enzymes are hydroxysteroid dehydrogenases (11β-HSDs; EC 1.1.1.146), which inter‐ convert inactive GCs and the active GCs (Gathercole & Stewart, 2010; Seckl & Walker, 2004; Stewart, 2005; Tomlinson et al., 2004).


Menopause | 2017

Natural mineral-rich water ingestion by ovariectomized fructose-fed Sprague-Dawley rats: effects on sirtuin 1 and glucocorticoid signaling pathways

Jugal Kishore Das; Milton Severo; Cidália Dionísio Pereira; Emília Patrício; José Magalhães; Rosário Monteiro; Delminda Neves; Maria João Martins

Objective: Prevention or induction of metabolic disorders and obesity depend on estrogen signaling and/or exogenous factors, such as mineral content in diet. The protective effects of a Portuguese natural mineral-rich water against the induction of metabolic syndrome in fructose-fed male Sprague-Dawley rats have been reported. The present study was designed to assess the impact of this mineral-rich water on fructose-fed estrogen-deficient female Sprague-Dawley rats. Methods: Ovariectomized rats had access to tap (TWO) or mineral-rich (MWO) waters, with and without 10% fructose (10-wk treatment). A sham-operated (tap water supplied) group was included and each of the five groups included six rats. Plasma biochemical and metabolic parameters were evaluated by routine clinical measurements. Western blotting was used to assess hepatic protein expression of sirtuins (Sirt) 1 and 3, phosphorylated AMP-activated protein kinase-&agr; (p-AMPK&agr;), peroxisome proliferator-activated receptor gamma coactivator-1-&agr; (PGC1&agr;), glucocorticoid receptor, and 11beta-hydroxysteroid dehydrogenase type 1 (11&bgr;HSD1). Results: Ovariectomy increased plasma total cholesterol (46%/P < 0.05), but had no significant effects on hepatic protein expression. Fructose intake by ovariectomized rats increased PGC1&agr; and 11&bgr;HSD1 (fructose in tap water [TWFO] vs TWO: 65%/P < 0.05 and 38%/P = 0.05, respectively) as well as glucocorticoid receptor (TWFO and fructose in natural mineral-rich water [MWFO] vs TWO and MWO: 107%/P = 0.05 and 182%/P < 0.05, respectively). Mineral-rich water ingestion exerted an increasing shape on Sirt1 (MWO vs TWO: 76%/P < 0.05; MWFO vs TWFO: 76%/P = 0.06), PGC1&agr; (MWO vs TWO: 77%/P < 0.01), p-AMPK&agr; (MWO vs TWO: 152%/P = 0.01; MWFO vs TWFO: 107%/P = 0.01), and 11&bgr;HSD1 (MWO vs TWO: 91%/P = 0.05; MWFO vs TWFO: 47%/P = 0.05). Conclusions: Mineral-rich water ingestion may have a prime role on the activation of Sirt1 signaling and the modulation of glucocorticoid signaling in the postmenopause.


Microscopy and Microanalysis | 2012

Effects of a Hypersaline Sodium-rich Carbonated Natural Mineral Water on Structure and Expression of VEGF, VEGFR1, VEGFR2, Ang1, Ang2 and Tie2 of Fructose-treated Rat Corpus Cavernosum

Delminda Neves; Inês Tomada; Cidália Dionísio Pereira; Rosário Monteiro; Maria João Martins

Metabolic Syndrome (MS) definition is based on a cluster of metabolic risk factors that identifies subjects at high risk for forthcoming type 2 diabetes mellitus and atherosclerotic cardiovascular diseases (CVD). Although the exact aetiology of the MS still remains unclear, it is known to involve complex interactions between genetic, metabolic and environmental factors, with diet and oxidative stress playing important roles. Regular increased fructose consumption has been associated to some metabolic adverse changes observed in the MS and, thus, fructose-fed is considered a suitable animal model of diet-induced MS. On the other hand, calcium, magnesium and potassium, generally deficient in MS-inducing diets, and abundant in natural mineral-rich waters, have been proposed protective against the MS. Although their exact effects are not yet fully clarified, natural mineral-rich waters present some antioxidant properties that exert protection against reactive oxygen species that are chief contributors to the increase of CVD risk, considering their reactivity to nitric oxide (NO). Such waters also improve some MS metabolic risk factors. Degradation of NO seriously compromises the vasodilatation mechanism leading to endothelial dysfunction, which always precedes atherosclerosis — the main contributor to CVD and erectile dysfunction. Penis erection is a vascular process that strongly depends on NO-induced smooth muscle relaxation. Moreover, NO mediates indirectly the vascular endothelial growth factor (VEGF)-induced angiogenesis, which is fundamental to maintain endothelium integrity in the cavernous tissue. VEGF binds specifically to VEGF tyrosine kinase membrane receptors (VEGFR1 and VEGFR2), and crosstalk in vivo with other angiogenic factors such as angiopoietins that compete for binding to the endothelial-specific Tie2 receptor. Previous work from our group demonstrated that long-term consumption of antioxidant-rich beverages modifies the expression of VEGF, Ang1, Ang2 and their receptors VEGFR1, VEGFR2 and Tie2 in the cavernous tissue of the rat, preventing atherosclerosis progression.

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