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Despite the several mismatches of methodological understanding between teachers and students in higher education, research methodologies in education are a relatively common pedagogical practice in most European advanced courses in education. However, only some studies have shown what pedagogical practices are mobilised by the teachers with their specific scientific conceptions. This article presents and discusses the results of an extensive research study conducted in Portugal with all the teachers involved in teaching research methodologies on master's and doctoral programmes in education. The results show the personal and professional characteristics of the teachers involved in this teaching and the type of senses, decisions, and challenges experienced when teaching research methodologies. The study identifies and characterises the research culture generated by the different pedagogical practices in this scientific field. Based on the results, we argue that the teachers' scientific conceptions and pedagogical practices may be developed by a "peer authorial construction of research understanding," aiming to provide appropriate educational experiences to students in research methodologies courses in advanced studies in education.

Despite the several mismatches of methodological understanding between teachers and students in higher education, research methodologies in education are a relatively common pedagogical practice in most European advanced courses in education. However, only some studies have shown what pedagogical practices are mobilised by the teachers with their specific scientific conceptions. This article presents and discusses the results of an extensive research study conducted in Portugal with all the teachers involved in teaching research methodologies on master’s and doctoral programmes in education. The results show the personal and professional characteristics of the teachers involved in this teaching and the type of senses, decisions, and challenges experienced when teaching research methodologies. The study identifies and characterises the research culture generated by the different pedagogical practices in this scientific field. Based on the results, we argue that the teachers’ scientific conceptions and pedagogical practices may be developed by a “peer authorial construction of research understanding,” aiming to provide appropriate educational experiences to students in research methodologies courses in advanced studies in education.

There is an urgent need for effective disease-modifying therapeutic interventions for Alzheimer’s disease (AD)—the most prevalent cause of dementia with a profound socioeconomic burden. Most clinical trials targeting the classical hallmarks of this disease—β-amyloid plaques and neurofibrillary tangles—failed, showed discrete clinical effects, or were accompanied by concerning side effects. There has been an ongoing search for novel therapeutic targets. Neuroinflammation, now widely recognized as a hallmark of all neurodegenerative diseases, has been proven to be a major contributor to AD pathology. Here, we summarize the role of neuroinflammation in the pathogenesis and progression of AD and discuss potential targets such as microglia, TREM2, the complement system, inflammasomes, and cytosolic DNA sensors. We also present an overview of ongoing studies targeting specific innate immune system components, highlighting the progress in this field of drug research while bringing attention to the delicate nature of innate immune modulations in AD.

Objectives: Metformin is the first line therapy recommended for type 2 diabetes. However, the precise mechanism of action remains unclear and up to a quarter of patients show some degree of intolerance to the drug, with a similar number showing poor response to treatment, limiting its effectiveness. A better understanding of the mechanism of action of metformin may improve its clinical use. SLC2A2 (GLUT2) is a transmembrane facilitated glucose transporter, with important roles in the liver, gut and pancreas. Our group previously identified single nucleotide polymorphisms in the human SLC2A2 gene, which were associated with reduced transporter expression and an improved response to metformin treatment. The aims of this study were to model Slc2a2 deficiency and measure the impact on glucose homoeostasis and metformin response in mice. Methods: We performed extensive metabolic phenotyping and 2-deoxy-2-[18F]fluoro-d-glucose ([18F]FDG)-positron emission tomography (PET) analysis of gut glucose uptake in high-fat diet-fed (HFD) mice with whole-body reduced Slc2a2 (Slc2a2+/−) and intestinal Slc2a2 KO, to assess the impact of metformin treatment. Results: Slc2a2 partial deficiency had no major impact on body weight and insulin sensitivity, however mice with whole-body reduced Slc2a2 expression (Slc2a2+/−) developed an age-related decline in glucose homoeostasis (as measured by glucose tolerance test) compared to wild-type (Slc2a2+/+) littermates. Glucose uptake into the gut from the circulation was enhanced by metformin exposure in Slc2a2+/+ animals fed HFD and this action of the drug was significantly higher in Slc2a2+/− animals. However, there was no effect of specifically knocking-out Slc2a2 in the mouse intestinal epithelial cells. Conclusions: Overall, this work identifies a differential metformin response, dependent on expression of the SLC2A2 glucose transporter, and also adds to the growing evidence that metformin efficacy includes modifying glucose transport in the gut. We also describe a novel and important role for this transporter in maintaining efficient glucose homoeostasis during ageing.

Chronic stress is a major risk factor for developing mental illnesses and cognitive deficiencies although stress-susceptibility varies individually. In a recent study, we established the connection between chronic social defeat stress (CSDS) and impaired motor learning abilities accompanied by chronically disturbed structural neuroplasticity in the primary motor cortex (M1) of mice. In this study, we further investigated the long-term effects of CSDS exposure on M1, focusing on the interneuronal cell population. We used repeated CSDS to elicit effects across behavioral, endocrinological, and metabolic parameters in mice. Susceptible and resilient phenotypes were discriminated by symptom load and motor learning abilities were assessed on the rotarod. Structural changes in interneuronal circuits of M1 were studied by immunohistochemistry using parvalbumin (PV+) and somatostatin (SST+) markers. Stress-susceptible mice had a blunted stress hormone response and impaired motor learning skills. These mice presented reduced numbers of both interneuron populations in M1 with layer-dependent distribution, while alterations in cell size and immunoreactivity were found in both susceptible and resilient individuals. These results, together with our previous data, suggest that stress-induced cell loss and degeneration of the GABAergic interneuronal network of M1 could underlay impaired motor learning, due to their role in controlling the excitatory output and spine dynamics of principal neurons required for this task. Our study further highlights the importance of long-term outcomes of chronically stressed individuals which are translationally important due to the long timecourses of stress-induced neuropsychiatric disorders.

Professor Catedrático da Universidade Lusófona de Humanidades e Tecnologias, em Lisboa. Doutor em Ciências da Educação pela Universidade Nova de Lisboa. Diretor do Centro de Estudos Interdisciplinares em Educação e Desenvolvimento (CeiED), da Universidade Lusófona. Vice-Presidente do Comitê de Investigação de Sociologia da Educação (RC04) da Associação Internacional de Sociologia (2006-2014). Co-fundador do Instituto Paulo Freire, de Portugal. Coordenador da Rede Ibero-Americana de Investigação em Políticas de Educação (RIAIPE). Fundador da Seção de Educação Comparada da Sociedade Portuguesa de Educação Comparada (SEC-SPCE). Membro do Comité Europeu da Confederação Mundial das Organizações da Profissão Docente, CMOPE/WCOTP (1988-1992) e do Comité Europeu da Internacional de Educação (1993-1994). Inspector-Chefe do Ensino Primário (1974-1975), membro do Conselho Nacional de Educação (1988-1994). Consultor do Conselho de Ministros para os Assuntos da Educação, Formação, Cultura e Ciência (1995-1999). Diretor da Revista Lusófona de Educação e membro do Conselho Editorial de dezenas de revistas em Portugal, Brasil, EUA e França. Foi membro fundador do movimento sindical docente, Presidente da Direção do Sindicato dos Professores da Grande Lisboa (1979-1989) e Secretário-Geral da Federação Nacional dos Professores, FENPROF (1983-1994).

With the continuous rise in the worldwide prevalence of obesity and type 2 diabetes, developing therapies regulating body weight and glycemia has become a matter of great concern. Among the current treatments, evidence now shows that the use of intestinal hormone analogs (e.g., GLP1 analogs and others) helps to control glycemia and reduces body weight. Indeed, intestinal endocrine cells produce a large variety of hormones regulating metabolism, including appetite, digestion, and glucose homeostasis. Herein, we discuss how the enteroendocrine system is affected by local environmental and metabolic signals. These signals include those arising from unbalanced diet, gut microbiota, and the host metabolic organs and their complex cross-talk with the intestinal barrier integrity.

This document is intended to represent the reality of Hospital Pedagogy in Venezuela. Its purpose is to provide a historical view first, of the most significant events that allowed the emergence, development and consolidation of Hospital Pedagogy in Venezuela, as well as the implementation and commissioning of the first hospital wards. Then, addressing teacher training in Hospital Pedagogy, he continues to research in the advancement of this type of education in our context, as well as the description of programs and projects conducted in the country for the benefit of the hospitalized population and the presentation of some final considerations.

Objective: Intestinal glucose absorption is orchestrated by specialized glucose transporters such as SGLT1 and GLUT2. However, the role of GLUT2 in the regulation of glucose absorption remains to be fully elucidated. Methods: We wanted to evaluate the role of GLUT2 on glucose absorption and glucose homeostasis after intestinal-specific deletion of GLUT2 in mice (GLUT2ΔIEC mice). Results: As anticipated, intestinal GLUT2 deletion provoked glucose malabsorption as visualized by the delay in the distribution of oral sugar in tissues. Consequences of intestinal GLUT2 deletion in GLUT2ΔIEC mice were limiting body weight gain despite normal food intake, improving glucose tolerance, and increasing ketone body production. These features were reminiscent of calorie restriction. Other adaptations to intestinal GLUT2 deletion were reduced microvillus length and altered gut microbiota composition, which was associated with improved inflammatory status. Moreover, a reduced density of glucagon-like peptide-1 (GLP-1) positive cells was compensated by increased GLP-1 content per L-cell, suggesting a preserved enteroendocrine function in GLUT2ΔIEC mice. Conclusions: Intestinal GLUT2 modulates glucose absorption and constitutes a control step for the distribution of dietary sugar to tissues. Consequently, metabolic and gut homeostasis are improved in the absence of functional GLUT2 in the intestine, thus mimicking calorie restriction. Author Video: Author Video Watch what authors say about their articles Keywords: Malabsorption, Glucose homeostasis, Intestinal adaptation, Microbiota, GLP-1

Enacted in 1966 by the Law 5.107 and currently dictated by the Law 8.036/90, the employee's dismissal fund (FGTS) works as a social nature fund to defray the housing and infrastructure system, and also to help the helplessness worker. Every monthly payment, compulsorily paid by the employer to every employee hired under employment laws (CLT), is deposited at CEF where the balance is updated by the Reference Rate (TR) plus an annual average interest rate of 3%. Since 1999, due to the gradual reduction of the Selic - the interest rate from which the TR is extracted - the employee's FGTS balance is being partially eroded for this monetary adjustment does not offset the inflation rate at some periods. This has entailed a surging amount of lawsuits with the aim of reverting occasional losses by the CLT employees in their FGTS accounts. This paper discusses the subject in the light of the workers' pleas and arguments, with special emphasis on its aspects and potential decisions on the subject.

The paper discusses the suitability of judicial mediation for the solution of labor disputes. Judicial and extrajudicial conflict-solving methods are approached, with emphasis on mediation. Aiming at understanding both the adequacy and application of mediation in Labor Law, the paper examines special principles of this branch, in particular, the principle of unavailability of Labor rights, for which the case of absolute and relative rights are contrasted. Finally, it concludes for the application of mediation to the Collective Labour Law, which is limited to the rights of relative unavailability.

Cuando se habla de terapias con animales, toda la literatura se vuelca en los beneficios del animal humano que participa de ellas, así como su comprobación científica, la óptica abarca también los posibles riesgos del humano con el contacto animal, inclusive los costos de dichas terapias, sin embargo, poca literatura analiza estas terapias con una óptica proteccionista del animal, siendo que es claro que en su mayoría, el afectado resulta siendo éste, pues suele ser apartado de su hábitat, sometido a entrenamientos crueles, a condiciones innaturales y de maltrato. El objetivo fundamental es visibilizar al animal como un ser vivo que siente, padece y que es merecedor de una serie de derechos que deben respetarse dentro de las terapias en que participa. Es por ello, que en esta ocasión, si bien la investigación parte de reconocer algunos beneficios de las terapias con animales, profundiza en aquellas características y condiciones que han de tener dichas terapias para que sean amigables con los animales que participan en ellas, constituyendo una lectura reflexiva y sensibilizadora, tanto para terapeutas, animalistas, pacientes y familiares. La revisión incluye un abordaje legal de la situación del maltrato animal y sus repercusiones en terapias con canes, delfines y equinos.

Cardiovascular magnetic resonance imaging (CMR) has become an indispensable clinical tool for the assessment of morphology, function and structure of the heart muscle. By exploiting quantification of the effective transverse relaxation time (T2*) CMR also affords myocardial tissue characterization and probing of cardiac physiology, both being in the focus of ongoing research. These developments are fueled by the move to ultrahigh magnetic field strengths, which permits enhanced sensitivity and spatial resolution that help to overcome limitations of current clinical MR systems with the goal to contribute to a better understanding of myocardial (patho)physiology in vivo. In this context, the aim of this report is to introduce myocardial T2* mapping at ultrahigh magnetic fields as a promising technique to non-invasively assess myocardial (patho)physiology. For this purpose the basic principles of T2* assessment, the biophysical mechanisms determining T2* and (pre)clinical applications of myocardial T2* mapping are presented. Technological challenges and solutions for T2* sensitized CMR at ultrahigh magnetic field strengths are discussed followed by a review of acquisition techniques and post-processing approaches. Preliminary results derived from myocardial T2* mapping in healthy subjects and cardiac patients at 7.0 T are presented. A concluding section discusses remaining questions and challenges and provides an outlook on future developments and potential clinical applications.

Este artigo apresenta os primeiros resultados de uma parceria, estabelecida em 2015, entre a Agência Universitária de Notícias (AUN) e o Sistema Integrado de Bibliotecas (SIBi), órgão gestor do Portal de Revistas da USP, com o objetivo de realizar ações de divulgação científica. Mídia mais antiga da Universidade de São Paulo, prestes a completar 50 anos de existência, a AUN organiza seu trabalho em alunos-setoristas, responsáveis pela cobertura da produção científica e cultural da instituição para a sociedade. A partir da iniciativa aqui relatada, a AUN passou a ter setoristas designados para cobrir a produção publicada nas revistas científicas da Universidade, ato que colaborou para a entrada do Portal de Revistas no Ranking Web of Repositories, mantido pelo Webometrics Ranking of World Universities, uma iniciativa do Cybermetrics Lab, grupo de pesquisa do Conselho Superior de Investigações Científicas (CSIC), da Espanha

O presente relato apresenta as principais atividades e desafios de um embedded librarian, ou bibliotecário integrado, junto aos diversos grupos envolvidos nos processos de comunicação científica e, mais especificamente, relacionados aos periódicos científicos da área de Psicologia. A existência de um bibliotecário integrado a esses grupos favoreceu a comunicação e interação entre eles e contribuiu também para a qualificação de um conjunto de periódicos científicos da área.

The enterohormone glucagon-like peptide-1 (GLP-1) is required to amplify glucose-induced insulin secretion that facilitates peripheral glucose utilisation. Alteration in GLP-1 secretion during obesity has been reported but is still controversial. Due to the high adaptability of intestinal cells to environmental changes, we hypothesised that the density of GLP-1-producing cells could be modified by nutritional factors to prevent the deterioration of metabolic condition in obesity. We quantified L-cell density in jejunum samples collected during Roux-en-Y gastric bypass in forty-nine severely obese subjects analysed according to their fat consumption. In mice, we deciphered the mechanisms by which a high-fat diet (HFD) makes an impact on enteroendocrine cell density and function. L-cell density in the jejunum was higher in obese subjects consuming >30 % fat compared with low fat eaters. Mice fed a HFD for 8 weeks displayed an increase in GLP-1-positive cells in the jejunum and colon accordingly to GLP-1 secretion. The regulation by the HFD appears specific to GLP-1-producing cells, as the number of PYY (peptide YY)-positive cells remained unchanged. Moreover, genetically obese ob/ob mice did not show alteration of GLP-1-positive cell density in the jejunum or colon, suggesting that obesity per se is not sufficient to trigger the mechanism. The higher L-cell density in HFD-fed mice involved a rise in L-cell terminal differentiation as witnessed by the increased expression of transcription factors downstream of neurogenin3 (Ngn3). We suggest that the observed increase in GLP-1-positive cell density triggered by high fat consumption in humans and mice might favour insulin secretion and therefore constitute an adaptive response of the intestine to balance diet-induced insulin resistance.

Regenerating (REG) proteins are associated with islet development, β-cell damage, diabetes and pancreatitis. Particularly, REG-1 and REG-3-beta are involved in cell growth/survival and/or inflammation and the Reg1 promoter contains interleukin-6 (IL-6)-responsive elements. We showed by transcriptome analysis that islets of Goto-Kakizaki (GK) rats, a model of spontaneous type 2 diabetes, overexpress Reg1, 3α, 3β and 3γ, vs Wistar islets. Goto-Kakizaki rat islets also exhibit increased cytokine/chemokine expression/release, particularly IL-6. Here we analyzed Reg1 and Reg3β expression and REG-1 immuno-localization in the GK rat pancreas in relationship with inflammation. Isolated pancreatic islets and acinar tissue from male adult Wistar and diabetic GK rats were used for quantitative RT-PCR analysis. REG-1 immunohistochemistry was performed on paraffin sections with a monoclonal anti-rat REG-1 antibody. Islet cytokine/chemokine release was measured after 48 h-culture. Islet macrophage-positive area was quantified on cryostat sections using anti-CD68 and major histocompatibility complex (MHC) class II antibodies. Pancreatic exocrine-to-endocrine Reg1 and Reg3β mRNA ratios were markedly increased in Wistar vs GK rats. Conversely, both genes were upregulated in isolated GK rat islets. These findings were unexpected, because Reg genes are expressed in the pancreatic acinar tissue. However, we observed REG-1 protein labeling in acinar peri-ductal tissue close to islets and around large, often disorganized, GK rat islets, which may retain acinar cells due to their irregular shape. These large islets also showed peri-islet macrophage infiltration and increased release of various cytokines/chemokines, particularly IL-6. Thus, IL-6 might potentially trigger acinar REG-1 expression and secretion in the vicinity of large diabetic GK rat islets. This increased acinar REG-1 expression might reflect an adaptive though unsuccessful response to deleterious microenvironment.

In previous work, we demonstrated that a 65% protein calorie food restriction started during the third trimester of gestation in rats caused a reduced [beta]-cell mass at 4 days of life that persisted until adult age. In this study with adult undernourished (U) rats, we investigated 1) whether undernutrition affects the [beta]-cell growth potential and both [beta]-cell proliferation and differentiation and 2) the implication of the IGFs, highly responsive to nutritional status, in these processes. To this end, we used the 90% pancreatectomy (Px) procedure in U and control (C) adult rats. The results show that, on day 2 after Px, [beta]-cell replication was significantly higher in C rats, whereas the [beta]-cell neogenesis was markedly increased in U/Px rats. Both the serum levels of IGF-I and the liver IGF-I mRNA expression were reduced in adult U rats before and after Px compared with C rats. Pancreatic IGF-I mRNA expression was reduced in U animals on day O. However, on day 2 after Px, the increase of pancreatic IGF-I mRNA expression was significantly higher in U rats than in C rats. These data suggest that [beta]-cells still have the capacity to regenerate in the adult U rats, with a higher efficiency than C rats on day 2, and that both [beta]-cell neogenesis and [beta]-cell replication are stimulated. The increased pancreatic IGF-I mRNA may be instrumental in these processes. [beta]-cell regeneration; proliferation; insulin-like growth factors

RESUMEN: Teniendo en cuenta las necesidades educativas del niño enfermo y a su vez la necesidad de compensar y normalizar en la medida de lo posible la situación de estos niños, presentamos los resultados obtenidos en la investigación que hemos llevado a cabo en el Hospital Clínico Universitario y el Hospital «Virgen de la Vega» de Salamanca, y que hace referencia a la situación y tratamiento de niños hospitalizados en edad escolar. Los resultados indican niveles moderados de ansiedad en los niños como un estado producto de su hospitalización, además estos resultados arrojaron diferencias significativas entre los niños que asisten al aula hospitalaria de los que no reciben ningún tipo de atención educativa en el estado de la ansiedad. De acuerdo a estos resultados y desde la perspectiva de la pedagogía hospitalaria, defendemos la necesidad de desarrollar programas de intervención educativa en el ámbito hospitalario como una alternativa en la reducción de la ansiedad infantil hospitalaria, por ser este trastorno uno de los más frecuentes dentro de las reacciones de los niños enfermos hospitalizados.ABSTRACT: Taking into account the educational needs of sick children and in turn, the need to compénsate and normalize the situation of these children as much as possible, we present the results obtained in the research we carried out in the University Clinical Hospital and the «Virgen de la Vega» Hospital in Salamanca. This research refers to the situation and treatment of school-aged hospitalised children. The results indícate modérate levéis of anxiety in the children as a condition produced by their hospitalisation. Furthermore, these results show significant differences in this state of anxiety between the children who attend the hospital classroom and those that receive no type of educational attention. In accordance with these results and from the perspective of hospital education, we defend the need to develop programmes of educational intervention in hospitals as an alternative for reducing hospitalised children's anxiety, since this condition is one of the most frequent reactions reported in these children.RÉSUMÉ: Nous presentons les resultats que nous avons obtenue a la investigation que nous avons fait dans les hópitals de Salamanca sur la situation des enfants hospitalisés. Nous avons découvert une grande ansieté, sur tous dans les enfants qui ne vont pas a l'école hospitalaire. Cést pour cela que nous demandons une terapie specifique pour compenser la situation d'ansieté á l'hópital.

RESUMEN: La incorporación de bibliotecas, así como el fomento de la lectura dentro de las instituciones hospitalarias es un área de interés creciente para las personas que nos dedicamos a la atención del niño hospitalizado en favor de su calidad de vida. Junto a las aportaciones teóricas derivadas de este enfoque, hay que resaltar la existencia de un cuerpo creciente de evidencia empírica y de importantes implicaciones en la práctica profesional. Teniendo en cuenta la necesidad de hacer más placentera la estancia hospitalaria, el artículo que se presenta se centra fundamentalmente en aportar una visión de la lectura como un instrumento de desarrollo personal y como medio para distraer y curar (biblioterapia) además de valorar el panorama de las iniciativas desarrolladas dentro del contexto hospitalario que se presentan como una necesidad a tener en cuenta y que urge desarrollar.ABSTRACT: The incorporation of libraries as well as the fostering of reading in hospital institutions form an area of growing interest for those devoted to improving the quality of life of hospitalised children. Together with the theoretical contributions deriving from this approach, it should be stressed that there is growing empirical evidence with important implications for professional practice. With a view to the need to make hospital stays more pleasant, the present article focuses mainly on giving a view of reading as an instrument for personal development and as a means to distract and cure (bibliotherapy), besides evaluating the panorama of the initiatives developed within the hospital context, which are presented as a need to be taken into account and which should urgently be developed.

BackgroundMammals must sense the amount of sugar available to them and respond appropriately. For many years attention has focused on intracellular glucose sensing derived from glucose metabolism. Here, we studied the detection of extracellular glucose concentrations in vivo by invalidating the transduction pathway downstream from the transporter-detector GLUT2 and measured the physiological impact of this pathway.Methodology/principal findingsWe produced mice that ubiquitously express the largest cytoplasmic loop of GLUT2, blocking glucose-mediated gene expression in vitro without affecting glucose metabolism. Impairment of GLUT2-mediated sugar detection transiently protected transgenic mice against starvation and streptozotocin-induced diabetes, suggesting that both low- and high-glucose concentrations were not detected. Transgenic mice favored lipid oxidation, and oral glucose was slowly cleared from blood due to low insulin production, despite massive urinary glucose excretion. Kidney adaptation was characterized by a lower rate of glucose reabsorption, whereas pancreatic adaptation was associated with a larger number of small islets.Conclusions/significanceMolecular invalidation of sugar sensing in GLUT2-loop transgenic mice changed multiple aspects of glucose homeostasis, highlighting by a top-down approach, the role of membrane glucose receptors as potential therapeutic targets.

The glucose of non-insulin dependent rat diabetic neonatal streptozotocin (nO-STZ) beta-cells does not activate adenylate cyclase due to a deficiency in the glucose metabolism of the cells. The deficient activation of adenylate cyclase is due to the inability of glucose in nO-STZ beta cells to generate sufficient levels of cytostolic Ca2+. Treatment of nO-STZ rat pancreatic islets with forskolin, glucagon, isobutyl methylxanthine and gastric inhibitory polypeptide enhanced adenylate cyclase activation.

The present study was designed to identify in a model of noninsulin-dependent diabetes induced by neonatal streptozotocin (n0-STZ), the long-term consequences of an islet graft upon 1) glucose handling of the recipient and, 2) glucose response of the residual β cells in the recipient pancreas. We have examined, 4 and 8 wk after islet implantation under the kidney capsule of syngeneic diabetic n0-STZ rats, their tolerance to glucose administered in vivo, together with their insulin release in response to glucose in vivo (oral glucose tolerance test) as well as in vitro (perfused pancreas). The results in the islet-grafted n0-STZ rats, were compared to those obtained in nongrafted nondiabetic rats and nongrafted n0-STZ rats. Our study shows that transplanting a limited number (900) of adult islets under the kidney capsule reverses to normal, many parameters of the noninsulin-dependent diabetic state in the n0-STZ rat model: these include body weight, basal plasma glucose in both the nonfasted and postabsorptive states, and basal plasma insulin in the postabsorptive state. Furthermore, tolerance to oral glucose administration was greatly improved in the transplanted rats and it was correlated with restoration of a manifest glucose-induced insulin secretion in vivo as evaluated (ΔI) during an oral glucose tolerance test. Our data clearly show that the insulin response to glucose from the endogenous pancreas of n0-STZ diabetic rat was not really improved by long-term (8 wk) basal normoglycemia. More precisely, we were able to detect a slight but significant improvement of the early phase of insulin release in vitro in response to glucose; however, the overall insulin response remained 15 times lower than the normal one with no reapparance of the late phase of insulin release. After cessation of glucose stimulation in vivo, off-response of insulin, which is also a landmark of the impaired insulin release by the β cells of n0-STZ rats, was still detectable in the perfused pancreas of the transplanted n0-STZ rats. Finally, because the reactivity to glucose of the endogenous residual β cells was not regained, the insulin released in vivo during the oral glucose test in the graft-bearing n0-STZ rats can be attributed mainly to functioning of the grafted islets population. Copyright © 1997 Elsevier Science Inc.

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The study of the gut microbiome holds great promise for understanding and treating metabolic diseases, as its functions and derived metabolites can influence the metabolic status of the host. While research on the fecal microbiome has provided valuable insights, it tells us only part of the story. This limitation arises from the substantial variations in microorganism distribution throughout the gastrointestinal tract due to changes in physicochemical conditions. Thus, relying solely on the fecal microbiome may not be sufficient to draw comprehensive conclusions about metabolic diseases. The proximal part of the small intestine, particularly the jejunum, indeed, serves as the crucial site for digestion and absorption of nutrients, suggesting a potential role of its microbiome in metabolic regulation. Unfortunately, it remains relatively underexplored due to limited accessibility. This review presents current evidence regarding the relationships between the microbiome in the upper small intestine and various phenotypes, focusing on obesity and type 2 diabetes, in both humans and rodents. Research on humans is still limited with variability in the population and methods used. Accordingly, to better understand the role of the whole gut microbiome in metabolic diseases, studies exploring the human microbiome in different niches are needed. [Display omitted] • Upper small intestine (USI) microbiome is crucial in nutrient absorption and digestion. • High-fat diet greatly impacts USI microbiome diversity and composition in rodents. • Bariatric surgery and inulin aid in the recovery of USI microbiome in HFD-fed mice • Metagenomic richness of USI microbiome inversely correlates with insulin resistance. • USI microbiome research in obesity is still limited and standardized methods are awaited. [ABSTRACT FROM AUTHOR]

Metformin is the first line therapy recommended for type 2 diabetes. However, the precise mechanism of action remains unclear and up to a quarter of patients show some degree of intolerance to the drug, with a similar number showing poor response to treatment, limiting its effectiveness. A better understanding of the mechanism of action of metformin may improve its clinical use. SLC2A2 (GLUT2) is a transmembrane facilitated glucose transporter, with important roles in the liver, gut and pancreas. Our group previously identified single nucleotide polymorphisms in the human SLC2A2 gene, which were associated with reduced transporter expression and an improved response to metformin treatment. The aims of this study were to model Slc2a2 deficiency and measure the impact on glucose homoeostasis and metformin response in mice. We performed extensive metabolic phenotyping and 2-deoxy-2-[18F]fluoro- d -glucose ([18F]FDG)-positron emission tomography (PET) analysis of gut glucose uptake in high-fat diet-fed (HFD) mice with whole-body reduced Slc2a2 (Slc2a2 +/− ) and intestinal Slc2a2 KO, to assess the impact of metformin treatment. Slc2a2 partial deficiency had no major impact on body weight and insulin sensitivity, however mice with whole-body reduced Slc2a2 expression (Slc2a2 +/− ) developed an age-related decline in glucose homoeostasis (as measured by glucose tolerance test) compared to wild-type (Slc2a2 +/+ ) littermates. Glucose uptake into the gut from the circulation was enhanced by metformin exposure in Slc2a2 +/+ animals fed HFD and this action of the drug was significantly higher in Slc2a2 +/− animals. However, there was no effect of specifically knocking-out Slc2a2 in the mouse intestinal epithelial cells. Overall, this work identifies a differential metformin response, dependent on expression of the SLC2A2 glucose transporter, and also adds to the growing evidence that metformin efficacy includes modifying glucose transport in the gut. We also describe a novel and important role for this transporter in maintaining efficient glucose homoeostasis during ageing. • Reducing GLUT2 in mice enhances response to the diabetes drug Metformin. • Less GLUT2 enhances Metformin induced glucose transport in the gut. • This does not need GLUT2 to be expressed in intestinal epithelial cells. • Less GLUT2 makes diabetes develop faster but gives better drug response. [ABSTRACT FROM AUTHOR]

Psicologia: Ciência e Profissão (PCP), publicada pelo Conselho Federal de Psicologia ao longo de 30 anos, registra o avanço da Psicologia, como ciência e profissão. O objetivo deste trabalho é relatar alguns aspectos que merecem destaque, a partir de 2005, quando PCP se consolida como uma revista científica, ganha a versão digital e se insere no movimento do acesso aberto. É feita também uma breve análise dos indicadores de citações da revista. As análises foram efetuadas a partir da leitura dos editoriais dos fascículos publicados do ano 2005 até o momento. Com base nos módulos de bibliometria do PePSIC e SciELO, além dos dados das referências da revista, foram levantados indicadores de citações recebidas e fornecidas por PCP. Os dados permitem afirmar que PCP vem aumentando o número de citações recebidas. A rede de revistas que mais citam PCP está publicada no PePSIC, demonstrando que publicações eletrônicas ganham maior visibilidade na comunidade científica. Ao completar 30 anos, a proposta da revista é o comprometimento com a Psicologia voltada para aliviar o sofrimento humano, mas também dedicada ao avanço da ciência psicológica. O conhecimento documentado em revistas científicas e o impacto que tais publicações representam para o saber universal é algo que deve ser abordado, discutido e entendido, assim, estudos dessa natureza devem ser incentivados.

Objective Intestinal glucose absorption is orchestrated by specialized glucose transporters such as SGLT1 and GLUT2. However, the role of GLUT2 in the regulation of glucose absorption remains to be fully elucidated. Methods We wanted to evaluate the role of GLUT2 on glucose absorption and glucose homeostasis after intestinal-specific deletion of GLUT2 in mice (GLUT2 ΔIEC mice). Results As anticipated, intestinal GLUT2 deletion provoked glucose malabsorption as visualized by the delay in the distribution of oral sugar in tissues. Consequences of intestinal GLUT2 deletion in GLUT2 ΔIEC mice were limiting body weight gain despite normal food intake, improving glucose tolerance, and increasing ketone body production. These features were reminiscent of calorie restriction. Other adaptations to intestinal GLUT2 deletion were reduced microvillus length and altered gut microbiota composition, which was associated with improved inflammatory status. Moreover, a reduced density of glucagon-like peptide-1 (GLP-1) positive cells was compensated by increased GLP-1 content per L-cell, suggesting a preserved enteroendocrine function in GLUT2 ΔIEC mice. Conclusions Intestinal GLUT2 modulates glucose absorption and constitutes a control step for the distribution of dietary sugar to tissues. Consequently, metabolic and gut homeostasis are improved in the absence of functional GLUT2 in the intestine, thus mimicking calorie restriction. [ABSTRACT FROM AUTHOR]