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Soriguer F.,Hospital Regional Universitario Carlos Haya | Valdes S.,Hospital Regional Universitario Carlos Haya | Morcillo S.,Fundacion Imabis | Esteva I.,Hospital Regional Universitario Carlos Haya | And 12 more authors.
European Journal of Clinical Investigation | Year: 2011

Background Different studies, mostly cross-sectional, have found an association between low levels of thyroid hormones, even within the normal range, and a greater body mass index. The aim of this study was to determine the association between thyroid function and the risk for obesity. Materials and methods In this population-based prospective study, measurements were made of anthropometric parameters, thyroid hormone function and urinary iodine in a cohort of the Pizarra Study (n=937), and repeated 6years later (n=784). At the second point, measurements were also made of leptin and adiponectin. Results Among the persons who were not obese at the start of the study, the odds ratio (OR) of becoming obese for those in the fourth quartile (Q 4) for free triiodothyronine (FT3) (versus those in Q 1) was 2·94 (1·46-5·90) (P=0·005). The OR of becoming obese in persons in Q 4 of FT4 (versus those in Q 1) was 3·06 (1·23-7·43) (P=0·01). Those persons in Q 4 of weight gain had a higher FT3 at the 6-year follow-up than those whose weight gain was in Q 1 (P<0·001). Leptin correlated with thyrotropin (β=0·58, P=0·001) and the FT4 (β=-1·12, P=0·005). Adiponectin correlated with FT3 (r=-0·24, P<0·001). The urinary iodine correlated negatively with both the BMI (β=-0·08, P=0·01) and the increase in weight (β=-0·08, P=0·04). Conclusions The changes in the thyroid hormones could be the consequence, rather than the cause, of the increase in weight. The same pathophysiological mechanisms that induce obesity might also be modifying the thyroid hormone pattern. © 2011 The Authors. European Journal of Clinical Investigation © 2011 Stichting European Society for Clinical Investigation Journal Foundation.

Mallol R.,Rovira i Virgili University | Rodriguez M.A.,Rovira i Virgili University | Brezmes J.,Rovira i Virgili University | Masana L.,CIBERDEM | And 2 more authors.
Progress in Nuclear Magnetic Resonance Spectroscopy | Year: 2013

NMR spectroscopy is the only technique that allows a full lipoprotein subfraction analysis of serum/plasma samples. The calibration and validation procedures used to set up new NMR methods rely on the correlations made between the NMR spectra and the lipids measured in a particular set of subfractions, all isolated by ultracentrifugation. Diffusion NMR spectroscopy can provide a direct measure of lipoprotein radii by using the diffusion coefficient and applying the Einstein Stokes equation. Nevertheless, the determination of the serum/plasma viscosity parameter in the formula is not straightforward. Many studies use NMR spectroscopy to characterize diabetic dyslipidemias. The number and size of the particles in the lipoprotein fractions provided by this technique have played an essential role in obtaining insight into this complex metabolic disease. Each NMR spectrum from a serum/plasma sample contains a wealth of information about lipoproteins.

Fuentes-Antras J.,Autonomous University of Madrid | Picatoste B.,Autonomous University of Madrid | Gomez-Hernandez A.,CIBERDEM | Gomez-Hernandez A.,Complutense University of Madrid | And 3 more authors.
Journal of Diabetes Research | Year: 2015

Diabetic cardiomyopathy entails a serious cardiac dysfunction induced by alterations in structure and contractility of the myocardium. This pathology is initiated by changes in energy substrates and occurs in the absence of atherothrombosis, hypertension, or other cardiomyopathies. Inflammation, hypertrophy, fibrosis, steatosis, and apoptosis in the myocardium have been studied in numerous diabetic experimental models in animals, mostly rodents. Type I and type II diabetes were induced by genetic manipulation, pancreatic toxins, and fat and sweet diets, and animals recapitulate the main features of human diabetes and related cardiomyopathy. In this review we update and discuss the main experimental models of diabetic cardiomyopathy, analysing the associated metabolic, structural, and functional abnormalities, and including current tools for detection of these responses. Also, novel experimental models based on genetic modifications of specific related genes have been discussed. The study of specific pathways or factors responsible for cardiac failures may be useful to design new pharmacological strategies for diabetic patients. © 2015 J. Fuentes-Antrás et al.

Flores L.,Obesity Unit | Vidal J.,Obesity Unit | Vidal J.,Institute dInvestigacions Biomediques August Pi i Sunyer | Canivell S.,CIBERDEM | And 6 more authors.
Surgery for Obesity and Related Diseases | Year: 2014

Background: There is scarce information about predictive factors of hypertension (HI) remission after bariatric surgery (BS). The aims of this study were to determine the clinical characteristics differentiating obese patients with and without HI and to evaluate the predictive factors associated with the risk of persistence of HI after BS.Patients and Methods: From January 2007 to December 2009, a review of patients who had undergone BS was performed. Patients were classified as hypertensive if having permanent use of antilll drugs or clinical BP ≥140/90 mm Hg. Weight, waist circumference (WC), and blood pressure were determined with standardized procedures.Results: Five hundred twenty-6 patients met the inclusion criteria; 264 (50%) were hypertensive, 74 (34%) of whom had type 2 diabetes. Before BS, older age, male gender, and greater WC differentiated hypertensive from normotensive patients. The prevalence of HI significantly fell to 35% (P < .0001) at 12 months after BS. The use of multivariate logistic regression showed that age >40, male gender and WC ≥ 130 cm were significant predictors of having HI before surgery. Regarding persistence of HI at the 12-month follow-up, the only independent predictors observed were time since diagnosis of HI > 10 years and the number of antilll drugs used. Presurgical BMI, WC, excess weight (EW), EW loss, surgical procedure, type 2 diabetes, and vitamin D status were not significant predictors.Conclusions: Bariatric surgery is associated with a high rate of HI remission. Older age, male gender, and higher WC differentiated hypertensive-obese from normotensive patients. After BS, longer duration and severity of HI were independently associated with no remission of HI. (Surg Obes Relat Dis 2014;10:661 665.). © 2014 American Society for Bariatric Surgery.

Pizarro-Delgado J.,Complutense University of Madrid | Fasciani I.,Ramon y Cajal Hospital IRYCIS | Temperan A.,Ramon y Cajal Hospital IRYCIS | Romero M.,Ramon y Cajal Hospital IRYCIS | And 16 more authors.
American Journal of Physiology - Endocrinology and Metabolism | Year: 2014

The existence of functional connexin36 (Cx36) hemichannels in β-cells was investigated in pancreatic islets of rat and wild-type (Cx36+/+), monoallelic (Cx36+/-), and biallelic (Cx36-/-) knockout mice. Hemichannel opening by KCl depolarization was studied by measuring ATP release and changes of intracellular ATP (ADP). Cx36+/+ islets lost ATP after depolarization with 70 mM KCl at 5 mM glucose; ATP loss was prevented by 8 and 20 mM glucose or 50 μM mefloquine (connexin inhibitor). ATP content was higher in Cx36-/- than Cx36+/+ islets and was not decreased by KCl depolarization; Cx36+/- islets showed values between that of control and homozygous isletFive minimolar extracellular ATP increased ATP content and ATP/ADP ratio and induced a biphasic insulin secretion in depolarized Cx36+/+ and Cx36+/- but not Cx36-/- islets. Cx36 hemichannels expressed in oocytes opened upon depolarization of membrane potential, and their activation was inhibited by mefloquine and glucose (IC50 ~8 mM). It is postulated that glucose-induced inhibition of Cx36 hemichannels in islet β-cells might avoid depolarization-induced ATP loss, allowing an optimum increase of the ATP/ADP ratio by sugar metabolism and a biphasic stimulation of insulin secretion. Gradual suppression of glucose-induced insulin release in Cx36+/- and Cx36-/- islets confirms that Cx36 gap junction channels are necessary for a full secretory stimulation and might account for the glucose intolerance observed in mice with defective Cx36 expression. Mefloquine targeting of Cx36 on both gap junctions and hemichannels also suppresses glucose-stimulated secretion. By contrast, glucose stimulation of insulin secretion requires Cx36 hemichannels' closure but keeping gap junction channels opened. © 2014 the American Physiological Society.

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