Sunshine vitamin and thyroid

Vitamin D exerts its canonical roles on the musculoskeletal system and in the calcium/phosphorus homeostasis. In the last years, increasing evidences suggested several extra-skeletal actions of this hormone, indicating that vitamin D may produce effects in almost all the body tissues. These are mediated by the presence of vitamin D receptor (VDR) and thanks to the presence of the 1-α-hydroxylase, the protein that converts the 25-hydroxyvitamin (calcidiol) to the active form 1,25-dihydroxyvitamin (calcitriol). Several studies evaluated the possible role of vitamin D in the pathogenesis of thyroid diseases, and this review will focus on the available data of the literature evaluating the association between vitamin D and thyroid function, vitamin D and autoimmune thyroid diseases, including Hashimoto's thyroiditis, Graves' disease and post-partum thyroiditis, and vitamin D and thyroid cancer

Obesity and Thyroid Cancer Risk: An Update

Thyroid cancer (TC) is the most common endocrine malignancy worldwide and its incidence has increased dramatically in recent years. In parallel, the prevalence of overweight and obesity has also increased, suggesting a possible link between these two diseases. Indeed, low-grade chronic inflammation, altered cytokine levels, insulin resistance, oxidative stress, and hormonal changes that occur in obese patients are all factors that contribute to the occurrence and growth of TC. In this review, the most recent evidence supporting the potential role of the mechanisms linking obesity to TC will be discusse

Association between Dietary Habits and Severity of Symptoms in Premenstrual Syndrome

Background. Premenstrual syndrome (PMS) is a set of physical, psychological, and emotional symptoms that occur during the luteal phase of the menstrual cycle. The etiopathogenesis of this condition is not fully understood, and several studies suggest a possible role of environmental factors, such as diet. The aim of this work was to investigate the relationship between dietary habits and the occurrence and severity of PMS. Methods and Results. Forty-seven women were enrolled in the study. Participants were asked to complete the Daily Record of Severity of Problems (DRSP) to diagnose PMS and to complete a three-day food record during the perimenstrual phase. Thirty women completed the study (16 with PMS and 14 controls). An analysis of the food diaries revealed no differences between the women with PMS and the control subjects in terms of total energy intake (1649 vs. 1570 kcal/day), diet composition, and the consumption of macro- or micronutrients, except for copper, whose consumption was higher in women with PMS than in the control subjects (1.27 ± 0.51 vs. 0.94 ± 0.49 mg/d, p < 0.05). Conclusions. The data presented here are very preliminary, and only a significant difference in copper intake was found when comparing women with PMS and controls. Larger studies are needed to better define how diet may contribute to the exacerbation of the psychological and somatic symptoms associated with PMS and whether PMS itself may influence macro- or micronutrient intake by changing dietary habits

Novel anti-obesity quercetin-derived Q2 prevents metabolic disorders in rats fed with high-fat diet

Objective: Obesity is often accompanied by an increased morbidity and mortality due to an increase of the cardiovascular disease risk factors, diabetes mellitus and dyslipidemia. Research is constantly working on protective molecules against obesity. In the present study, a novel Quercetin derivative Q2 was synthesized to overcome the poor bioavailability and low stability of Quercetin, a natural flavonoid with antioxidative and antiobesity properties. Methods: Rats were fed (12ws) with normodiet (fat:INS; 6.2%), High Fat Diet (fat:60%), HFDINS; +INS; Q2 in water (500INS; nM). Metabolic and anthropometric parameters were measured. 3T3-L1 preadipocytes were incubated with Q2 (1-25μM) and the differentiation program was evaluated by lipid accumulation through ORO staining. Gene and protein expression levels were assessed by RT-PCR and Western blot analysis. Results: Compared to HFD, HFDINS; +INS; Q2 rats showed reduced body weight, abdominal obesity, dyslipidemia and improved glucose tolerance. This is associated to lower adipose and liver modifications compared to hypertrophy and steatosis observed in HFD. In 3T3-L1 cells, lipid accumulation was significantly impaired by treatment with Q2. Indeed, Q2 significantly decreased the expression of the main adipogenic markers, c/EBPα and PPARγ both at mRNA and protein level. Conclusions: Our results indicate that Q2 markedly decreases differentiation of 3T3-L1 preadipocytes and contributes to prevent metabolic disorders as well as adipose and liver alterations typical of severe obesity induced by a HFD

Il confronto europeo sulle misure di PE

La Sezione 1.2, si apre con una breve presentazione degli indicatori di PE - consensuali e basati sulla spesa - adottati nei diversi paesi EU e dei dataset disponibili per la loro implementazione; vengono confrontati i risultati, anche alla luce delle evidenze da altre due misure - la soglia del 10% e l’indice Faiella-Lavecchia (2015) - e discussa la multidimensionalità del fenomeno

Thinking about accessibility in university education: conceptions and perspectives in dialogue with experience

En este artículo queremos compartir la experiencia de trabajar en perspectiva de accesibilidad desde la reflexión de la experiencia como también dar cuenta del proceso de construcción y transformación que venimos transitando en clave de pensar la accesibilidad y el derecho a la educación superior. Nos interesa abordar la estrategia institucional que tiene como objetivo integrar a los estudiantes, que presentan alguna discapacidad ya sea permanente o transitoria, a la universidad a través de acciones concretas que favorezcan la inclusión y den la bienvenida a “nuevos sujetos” con problemáticas particulares que interpelan a la institución en su todo complejo (Arendt, 2005). Compartir la experiencia de un programa de tutorías de accesibilidad, integrando un trabajo colaborativo y conjunto entre docentes, estudiantes, reconociendo en este espacio una experiencia que incluye y nos hace re-pensar el sentido de formarse y transitar la universidad pública. Pensar una estrategia de trabajo institucional que contribuya a ampliar y complejizar los marcos y bordes institucionales que aporten a una educación pública accesible, a la diversidad de colectivos que la componen.In this article we want to share the experience of working from an accessibility perspective from the reflection of the experience as well as to account for the construction and transformation process that we have been going through in terms of thinking about accessibility and the right to higher education. We are interested in addressing the institutional strategy that aims to integrate students, who present some permanent or temporary disability, to the university through concrete actions that favor inclusion and welcome “new subjects” with particular problems that they question the institution in its entire complex (Arendt, 2005). Sharing the experience of an accessibility tutorial program, integrating collaborative and joint work between teachers and students, recognizing in this space an experience that includes and makes us rethink the meaning of training and transiting the public university. Think of an institutional work strategy that contributes to expanding and making the institutional frameworks and borders more complex that contribute to an accessible public education, to the diversity of groups that compose it.Especialización en Docencia Universitari

Novel Findings into AIRE Genetics and Functioning: Clinical Implications

Autoimmune polyendocrinopathy candidiasis ectodermal dystrophy (APECED), formerly known as autoimmune polyendocrine syndrome type 1, is a paradigm of a monogenic autoimmune disease caused by mutations of a gene, named autoimmune regulator (AIRE). AIRE acts as a transcription regulator that promotes immunological central tolerance by inducing the ectopic thymic expression of many tissue-specific antigens. Although the syndrome is a monogenic disease, it is characterized by a wide variability of the clinical expression with no significant correlation between genotype and phenotype. Indeed, many aspects regarding the exact role of AIRE and APECED pathogenesis still remain unraveled. In the last decades, several studies in APECED and in its mouse experimental counterpart have revealed new insights on how immune system learns self-tolerance. Moreover, novel interesting findings have extended our understanding of AIRE's function and regulation thus improving our knowledge on the pathogenesis of APECED. In this review, we will summarize recent novelties on molecular mechanisms underlying the development of APECED and their clinical implications

Thinking about accessibility in university education: conceptions and perspectives in dialogue with experience

En este artículo queremos compartir la experiencia de trabajar en perspectiva de accesibilidad desde la reflexión de la experiencia como también dar cuenta del proceso de construcción y transformación que venimos transitando en clave de pensar la accesibilidad y el derecho a la educación superior. Nos interesa abordar la estrategia institucional que tiene como objetivo integrar a los estudiantes, que presentan alguna discapacidad ya sea permanente o transitoria, a la universidad a través de acciones concretas que favorezcan la inclusión y den la bienvenida a “nuevos sujetos” con problemáticas particulares que interpelan a la institución en su todo complejo (Arendt, 2005). Compartir la experiencia de un programa de tutorías de accesibilidad, integrando un trabajo colaborativo y conjunto entre docentes, estudiantes, reconociendo en este espacio una experiencia que incluye y nos hace re-pensar el sentido de formarse y transitar la universidad pública. Pensar una estrategia de trabajo institucional que contribuya a ampliar y complejizar los marcos y bordes institucionales que aporten a una educación pública accesible, a la diversidad de colectivos que la componen.In this article we want to share the experience of working from an accessibility perspective from the reflection of the experience as well as to account for the construction and transformation process that we have been going through in terms of thinking about accessibility and the right to higher education. We are interested in addressing the institutional strategy that aims to integrate students, who present some permanent or temporary disability, to the university through concrete actions that favor inclusion and welcome “new subjects” with particular problems that they question the institution in its entire complex (Arendt, 2005). Sharing the experience of an accessibility tutorial program, integrating collaborative and joint work between teachers and students, recognizing in this space an experience that includes and makes us rethink the meaning of training and transiting the public university. Think of an institutional work strategy that contributes to expanding and making the institutional frameworks and borders more complex that contribute to an accessible public education, to the diversity of groups that compose it.Especialización en Docencia Universitari

Glucose regulates diacylglycerol intracellular levels and protein kinase C activity by modulating diacylglycerol kinase subcellular localization.

Although chronic hyperglycemia reduces insulin sensitivity and leads to impaired glucose utilization, short term exposure to high glucose causes cellular responses positively regulating its own metabolism. We show that exposure of L6 myotubes overexpressing human insulin receptors to 25 mm glucose for 5 min decreased the intracellular levels of diacylglycerol (DAG). This was paralleled by transient activation of diacylglycerol kinase (DGK) and of insulin receptor signaling. Following 30-min exposure, however, both DAG levels and DGK activity returned close to basal levels. Moreover, the acute effect of glucose on DAG removal was inhibited by >85% by the DGK inhibitor R59949. DGK inhibition was also accompanied by increased protein kinase C-alpha (PKCalpha) activity, reduced glucose-induced insulin receptor activation, and GLUT4 translocation. Glucose exposure transiently redistributed DGK isoforms alpha and delta, from the prevalent cytosolic localization to the plasma membrane fraction. However, antisense silencing of DGKdelta, but not of DGKalpha expression, was sufficient to prevent the effect of high glucose on PKCalpha activity, insulin receptor signaling, and glucose uptake. Thus, the short term exposure of skeletal muscle cells to glucose causes a rapid induction of DGK, followed by a reduction of PKCalpha activity and transactivation of the insulin receptor signaling. The latter may mediate, at least in part, glucose induction of its own metabolism

Prep1 Controls Insulin Glucoregulatory Function in Liver by Transcriptional Targeting of SHP1 Tyrosine Phosphatase

AbstractObjective. We have investigated the function of the Prep1 gene in insulin-dependent glucose homeostasis in liver. Research design and methods. Prep1 action on insulin glucoregulatory function has been analyzed in liver of Prep1-hypomorphic mice (Prep1(i/i)), which express 2 to 3% of Prep1 mRNA. Results. Based on euglycemic hyperinsulinemic clamp studies, pyruvate tolerance tests and measurement of glycogen content, livers from Prep1(i/i) mice feature increased sensitivity to insulin. Tyrosine phosphorylation of both insulin receptor (IR) and IRS1/2 was significantly enhanced in Prep1(i/i) livers accompanied by a specific down-regulation of the SYP and SHP1 tyrosine phosphatases. Prep1 overexpression in HepG2 liver cells upregulated SYP and SHP1 and inhibited insulin-induced IR and IRS1/2 phosphorylation and was accompanied by reduced glycogen content. Consistently, overexpression of the Prep1 partner Pbx1 but not of p160MBP, mimicked Prep1 effects on tyrosine phosphorylations, glycogen content and on SYP and SHP1 expression. In Prep1 overexpressing cells, antisense silencing of SHP1, but not that of SYP, rescued insulin-dependent IR phosphorylation and glycogen accumulation. Both Prep1 and Pbx1 bind SHP1 promoter at a site located between nt -2113 and -1778. This fragment features enhancer activity and induces luciferase function by 7, 6 and 30-fold, respectively, in response to Prep1, Pbx1 or both. Conclusions. SHP1, a known silencer of insulin signal, is a transcriptional target of Prep1. In liver, transcriptional activation of SHP1 gene by Prep1 attenuates insulin signal transduction and reduces glucose storage