Elaboración de una escala de puntuación predictiva de infección periamigdalina basada en signos y síntomas / Design of a predictive score table for peritonsillar infection based on signs and symptoms

Introducción La infección periamigdalina (IPA) supone un motivo de consulta urgente entre las molestias de garganta. Un diagnóstico diferido o incorrecto puede comprometer la vía aerodigestiva alta y resultar mortal en su evolución. Nuestro objetivo fue desarrollar un modelo predictivo de presencia de IPA que ayude en su rápida detección. Pacientes y métodos Un estudio observacional retrospectivo de 66 meses desde 2017 fue desarrollado en un hospital comarcal y su centro terciario de referencia, recogiendo datos de todos los pacientes diagnosticados de IPA y un volumen proporcional de sujetos con sintomatología faríngea sin IPA. Recopilación de datos clínicos, exploratorios y demográficos entre participantes. Su mayor riesgo relativo de presencia de IPA los etiquetó como variables a testar. Elaboración de una escala de puntuación de probabilidad de padecerla y análisis de regresión logística, con obtención de la curva ROC que ofreciera mejor correlación diagnóstica. Validación interna y cálculo de los valores predictivos de este modelo. Resultados Sobre 348 casos de IPA, la escala de valoración puntuó la presencia de 6 variables: trismus (3), disfagia-odinofagia unilateral (2), abombamiento velar (2), otalgia refleja (1), faringolalia (1) y edad de 16-46 años (1). Con un rango de 0 a 10, un cut-off≥6 ofreció una sensibilidad del 96,1%, una especificidad del 93,9% y una eficienca del 94,9%. El área bajo la curva ROC fue de 0,979. Conclusiones La validación interna de este modelo basado en signos y síntomas la faculta como herramienta muy útil para detectar precozmente IPA en otorrinolaringología y atención primaria (AU)

Background Peritonsillar infection (PTI) is a reason for urgent consultation due to intense throat discomfort. A delayed or inaccurate diagnosis can jeopardize the upper aerodigestive tract and be fatal in its evolution. Our objective was to develop a predictive model for the presence of IPA helping in its rapid detection. Patients and methods A 66-month retrospective observational study from 2017 was carried out in a county and tertiary referral hospitals, registering data from all patients diagnosed with PTI and a proportional volume of subjects with pharyngeal symptoms without PTI. Collection of clinical, exploratory and demographic data among participants. Their higher relative risk of PTI presence allowed them to be considered as variables to be tested. Development of a scoring scale for the probability of suffering from it and logistic regression analysis, obtaining the ROC curve with the best diagnostic correlation. Internal validation and estimation of the predictive values of the model. Results On 348 cases of PTI, the assessment scale scored the presence of six variables: trismus (3), unilateral dysphagia-odynophagia (2), velar bulging (2), reflex otalgia (1), pharyngolalia (1) and age between 16 and 46 years (1). With a range of 0-10, a cut-off ≥6 offered a sensitivity of 96.1%, a specificity of 93.9%, and an efficiency of 94.9%. The area under the ROC curve was 0.979. Conclusions The internal validation of this model based on signs and symptoms makes it a very useful tool for early detection of PTI in otorhinolaryngology and primary care (AU)

[Design of a predictive score table for peritonsillar infection based on signs and symptoms]. / Elaboración de una escala de puntuación predictiva de infección periamigdalina basada en signos y síntomas.

BACKGROUND: Peritonsillar infection (PTI) is a reason for urgent consultation due to intense throat discomfort. A delayed or inaccurate diagnosis can jeopardize the upper aerodigestive tract and be fatal in its evolution. Our objective was to develop a predictive model for the presence of IPA helping in its rapid detection. PATIENTS AND METHODS: A 66-month retrospective observational study from 2017 was carried out in a county and tertiary referral hospitals, registering data from all patients diagnosed with PTI and a proportional volume of subjects with pharyngeal symptoms without PTI. Collection of clinical, exploratory and demographic data among participants. Their higher relative risk of PTI presence allowed them to be considered as variables to be tested. Development of a scoring scale for the probability of suffering from it and logistic regression analysis, obtaining the ROC curve with the best diagnostic correlation. Internal validation and estimation of the predictive values of the model. RESULTS: On 348 cases of PTI, the assessment scale scored the presence of six variables: trismus (3), unilateral dysphagia-odynophagia (2), velar bulging (2), reflex otalgia (1), pharyngolalia (1) and age between 16 and 46 years (1). With a range of 0-10, a cut-off ≥6 offered a sensitivity of 96.1%, a specificity of 93.9%, and an efficiency of 94.9%. The area under the ROC curve was 0.979. CONCLUSIONS: The internal validation of this model based on signs and symptoms makes it a very useful tool for early detection of PTI in otorhinolaryngology and primary care.

Estudio observacional prospectivo unicéntrico sobre el efecto de la prehabilitación trimodal en cirugía colorrectal / A single-center prospective observational study on the effect of trimodal prehabilitation in colorectal surgery

INTRODUCCIÓN: Se ha diseñado un protocolo de prehabilitación trimodal con el objetivo de valorar si contribuye a disminuir la morbilidad postoperatoria, valorar el efecto de la prehabilitación en la estancia hospitalaria global y analizar la evolución de la capacidad funcional antes y después de cirugía. MÉTODOS: Estudio observacional unicéntrico con pacientes con cáncer colorrectal intervenidos quirúrgicamente con intención curativa después de un protocolo de prehabilitación trimodal. Se recoge morbilidad postoperatoria según el Comprehensive Complication Index y estancia hospitalaria, y se compara con una matriz histórica. También se recoge capacidad funcional antes y después de la aplicación del protocolo de prehabilitación. RESULTADOS: En comparación con la población histórica se consigue disminuir el Comprehensive Complication Index global de forma estadísticamente significativa de 13,2 a 11,5. Desglosando por tipo de morbilidad, todas disminuyen en porcentaje sin conseguir significación (infección espacio quirúrgico del 11,7 al 8,4%; infección nosocomial del 15,8 al 10%, y morbilidad médica del 8,6 al 4,2%). La estancia hospitalaria global pasa de 6 a 4 días y el porcentaje de pacientes que se preparan en casa disminuye de forma estadísticamente significativa en ambos casos. CONCLUSIONES: La prehabilitación trimodal puede contribuir a disminuir la morbilidad postoperatoria y la estancia hospitalaria global de los pacientes intervenidos de neoplasia colorrectal

INTRODUCTION: A trimodal prehabilitation protocol was designed with the aim to evaluate whether it contributes to reducing postoperative morbidity, to evaluate the effect of prehabilitation on overall hospital stay, and to analyze the evolution of functional capacity before and after surgery. METHODS: A single-center observational study of patients with colorectal cancer who underwent surgery with curative intent after a trimodal prehabilitation protocol. We collected data for postoperative morbidity according to the Comprehensive Complication Index and hospital stay, which were compared with a historical matrix. Functional capacity data were also collected before and after the application of the prehabilitation protocol. RESULTS: Compared to the historical population, the overall Comprehensive Complication Index was reduced from 13.2 to 11.5, which was statistically significant. Analyzed by morbidity type, all decreased in percentage, although without achieving significance (surgical site infection from 11.7% to 8.4%, nosocomial infection 15.8 to 10% and medical morbidity 8.6% to 4.2%). The overall hospital stay went from 6 to 4 days, and the decrease in the percentage of patients who prepared at home was statistically significant in both cases. CONCLUSIONS: Trimodal prehabilitation can contribute to lowering the postoperative morbidity and overall hospital stay of patients undergoing colorectal cancer surgery

A single-center prospective observational study on the effect of trimodal prehabilitation in colorectal surgery. / Estudio observacional prospectivo unicéntrico sobre el efecto de la prehabilitación trimodal en cirugía colorrectal.

INTRODUCTION: A trimodal prehabilitation protocol was designed with the aim to evaluate whether it contributes to reducing postoperative morbidity, to evaluate the effect of prehabilitation on overall hospital stay, and to analyze the evolution of functional capacity before and after surgery. METHODS: A single-center observational study of patients with colorectal cancer who underwent surgery with curative intent after a trimodal prehabilitation protocol. We collected data for postoperative morbidity according to the Comprehensive Complication Index and hospital stay, which were compared with a historical matrix. Functional capacity data were also collected before and after the application of the prehabilitation protocol. RESULTS: Compared to the historical population, the overall Comprehensive Complication Index was reduced from 13.2 to 11.5, which was statistically significant. Analyzed by morbidity type, all decreased in percentage, although without achieving significance (surgical site infection from 11.7% to 8.4%, nosocomial infection 15.8 to 10% and medical morbidity 8.6% to 4.2%). The overall hospital stay went from 6 to 4 days, and the decrease in the percentage of patients who prepared at home was statistically significant in both cases. CONCLUSIONS: Trimodal prehabilitation can contribute to lowering the postoperative morbidity and overall hospital stay of patients undergoing colorectal cancer surgery.

Role of ghrelin isoforms in the mitigation of hepatic inflammation, mitochondrial dysfunction, and endoplasmic reticulum stress after bariatric surgery in rats.

BACKGROUND/OBJECTIVES: Bariatric surgery improves nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH), but the underlying mechanisms remain elusive. We evaluated the potential role of ghrelin isoforms in the amelioration of hepatic inflammation after sleeve gastrectomy and Roux-en-Y gastric bypass (RYGB). SUBJECTS/METHODS: Plasma ghrelin isoforms were measured in male Wistar rats (n = 129) subjected to surgical (sham operation, sleeve gastrectomy, or RYGB) or dietary interventions [fed ad libitum a normal (ND) or a high-fat diet (HFD) or pair-fed diet]. The effect of acylated and desacyl ghrelin on markers of inflammation, mitochondrial dysfunction, and endoplasmic reticulum (ER) stress in primary rat hepatocytes under palmitate-induced lipotoxic conditions was assessed. RESULTS: Plasma desacyl ghrelin was decreased after sleeve gastrectomy and RYGB, whereas the acylated/desacyl ghrelin ratio was augmented. Both surgeries diminished obesity-associated hepatic steatosis, CD68+- and apoptotic cells, proinflammatory JNK activation, and Crp, Tnf, and Il6 transcripts. Moreover, a postsurgical amelioration in the mitochondrial DNA content, oxidative phosphorylation (OXPHOS) complexes I and II, and ER stress markers was observed. Specifically, following bariatric surgery GRP78, spliced XBP-1, ATF4, and CHOP levels were reduced, as were phosphorylated eIF2α. Interestingly, acylated and desacyl ghrelin inhibited steatosis and inflammation of palmitate-treated hepatocytes in parallel to an upregulation of OXPHOS complexes II, III, and V, and a downregulation of ER stress transducers IRE1α, PERK, ATF6, their downstream effectors, ATF4 and CHOP, as well as chaperone GRP78. CONCLUSIONS: Our data suggest that the increased relative acylated ghrelin levels after bariatric surgery might contribute to mitigate obesity-associated hepatic inflammation, mitochondrial dysfunction, and ER stress.

Fatal anaphylactic shock induced by intravenous gelatin colloid: a postmortem allergological work-up

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Targeted disruption of the iNOS gene improves adipose tissue inflammation and fibrosis in leptin-deficient ob/ob mice: role of tenascin C.

BACKGROUND/OBJECTIVES: Obesity is related to a dynamic extracellular matrix (ECM) remodeling, which involves the synthesis and degradation of different proteins, such as tenascin C (TNC) in the adipose tissue (AT). Given the functional relationship between leptin and inducible nitric oxide synthase (iNOS), our aim was to analyze the impact of the absence of the iNOS gene in AT inflammation and ECM remodeling in ob/ob mice. SUBJECTS/METHODS: The expression of genes involved in inflammation and ECM remodeling was evaluated in 10-week-old male double knockout (DBKO) mice simultaneously lacking the ob and iNOS genes as well as in ob/ob mice classified into three groups [control, leptin-treated (1 mg kg-1 day-1) and pair-fed]. RESULTS: Leptin deficiency increased inflammation and fibrosis in AT. As expected, leptin treatment improved the obesity phenotype. iNOS deficiency in ob/ob mice improved insulin sensitivity, AT inflammation, and ECM remodeling, as evidenced by lower AT macrophage infiltration and collagen deposition, a downregulation of proinflammatory and profibrogenic genes Tnf, Emr1, Hif1a, Col6a1, Col6a3, and Tnc, as well as lower circulating TNC levels. Interestingly, leptin upregulated TNC expression and release in 3T3-L1 adipocytes, and iNOS knockdown in 3T3-L1 fat cells produced a significant decrease in basal and leptin-induced Tnc expression. CONCLUSIONS: Ablation of iNOS in leptin-deficient mice improved AT inflammation and ECM remodeling-related genes, attenuating fibrosis, and metabolic dysfunction. The activation of iNOS by leptin is necessary for the synthesis and secretion of TNC in adipocytes, suggesting an important role of this alarmin in the development of AT inflammation and fibrosis.

Role of aquaporin-7 in ghrelin- and GLP-1-induced improvement of pancreatic ß-cell function after sleeve gastrectomy in obese rats.

BACKGROUND/OBJECTIVES: Glycerol is a key metabolite for lipid accumulation in insulin-sensitive tissues as well as for pancreatic insulin secretion. We examined the role of aquaporin-7 (AQP7), the main glycerol channel in ß-cells, and AQP12, an aquaporin related to pancreatic damage, in the improvement of pancreatic function and steatosis after sleeve gastrectomy in diet-induced obese rats. SUBJECTS/METHODS: Male Wistar obese rats (n=125) were subjected to surgical (sham operation and sleeve gastrectomy) or dietary (pair-fed to the amount of food eaten by sleeve-gastrectomized animals) interventions. The tissue distribution and expression of AQPs in the rat pancreas were analyzed by real-time PCR, western blotting and immunohistochemistry. The effect of ghrelin isoforms and glucagon-like peptide 1 (GLP-1) on insulin secretion, triacylglycerol (TG) accumulation and AQP expression was determined in vitro in RIN-m5F ß-cells. RESULTS: Sleeve gastrectomy reduced pancreatic ß-cell apoptosis, steatosis and insulin secretion. Lower ghrelin and higher GLP-1 concentrations were also found after bariatric surgery. Acylated and desacyl ghrelin increased TG content, whereas GLP-1 increased insulin release in RIN-m5F ß-cells. Sleeve gastrectomy was associated with an upregulation of AQP7 together with a normalization of the increased AQP12 levels in the rat pancreas. Interestingly, ghrelin and GLP-1 repressed AQP7 and AQP12 expression in RIN-m5F ß-cells. AQP7 protein was negatively correlated with intracellular lipid accumulation in acylated ghrelin-treated cells and with insulin release in GLP-1-stimulated ß-cells. CONCLUSIONS: AQP7 upregulation in ß-cells after sleeve gastrectomy contributes, in part, to the improvement of pancreatic steatosis and insulin secretion by increasing intracellular glycerol used for insulin release triggered by GLP-1 rather than for ghrelin-induced TG biosynthesis.

Crosstalk between adipokines and myokines in fat browning.

Skeletal muscle is the largest organ determining whole-body insulin sensitivity and metabolic homoeostasis. Adaptive changes of skeletal muscle in response to physical activity include adjustments in the production and secretion of muscle-derived bioactive factors, known as myokines, such as myostatin, IL-4, IL-6, IL-7 and IL-15, myonectin, follistatin-like 1 or leukaemia inhibitory factor. These myokines not only act locally in the muscle in an autocrine/paracrine manner, but also are released to the bloodstream as endocrine factors to regulate physiological processes in other tissues. Irisin, derived from the cleavage of FNDC5 protein, constitutes a myokine that induces myogenesis and fat browning (switch of white adipocytes to brown fat-like cells) together with a concomitant increase in energy expenditure. Besides being a target for irisin actions, the adipose tissue also constitutes a production site of FNDC5. Interestingly, irisin secretion from subcutaneous and visceral fat depots is decreased by long-term exercise training and fasting, suggesting a discordant regulation of FNDC5/irisin in skeletal muscle and adipose tissue. Accordingly, our group has recently reported that the adipokine leptin differentially regulates FNDC5/irisin expression in skeletal muscle and fat, confirming the crosstalk between both tissues. Moreover, irisin secretion and function are regulated by other myokines, such as follistatin or myostatin, as well as by other adipokines, including fibroblast growth factor 21 and leptin. Taken together, myokines have emerged as novel molecular mediators of fat browning and their activity can be modulated by adipokines, confirming the crosstalk between skeletal muscle and adipose tissue to regulate thermogenesis and energy expenditure.

[Medication reconciliation at hospital admission: Results and identification of target patients]. / Conciliación de la medicación al ingreso: resultados e identificación de pacientes diana.

OBJECTIVE: To quantify and to classify the discrepancies between the admission treatment and the usual patient treatment. To determine the variables that predict those patients that will have more benefit from medication reconciliation. MATERIAL AND METHODS: A prospective medication reconciliation study was conducted in the Vascular Surgery Unit from March 2014 to December 2014. When the patients were admitted to the Vascular Surgery Unit, they were informed about the study and asked to prepare information about their chronic treatment. The pharmacist then checked their clinical records, outpatient prescriptions, and also interviewed the patient, obtaining the best pharmacotherapeutic history available. The discrepancies with the admission treatment were written into the patient electronic clinical records. Finally, the physician classified the discrepancies, and changed the treatment, if needed. The statistical analysis included a comparison between patients with and without a non-justified discrepancy (NJD). The statistically different characteristics were used to plot Receiver Operating Characteristic curves, in order to determine the sensitivity and the specificity of these variables to select patients with discrepancies. RESULTS: A total of 380 patients were included. There were 845 non-justified, 600 justified non-documented, and 439 justified documented discrepancies. At least one NJD was identified in 293 patients (77%), with 65 patients (17%) having only justified discrepancies, and 22 patients (6%) having no discrepancies. NJD were: different dose, route or schedule (51%), omission (39%), wrong drug (8%) and commission (2%). The variables associated with discrepancies were number of chronic medications drugs and provider of information. CONCLUSIONS: In most studies, omission is the most frequent error. In contrast, in our study the most frequent error is different dose, route, or schedule. The variable that allows selecting patients at higher risk of discrepancies is the number of chronic drugs. This risk is also increased if the patients are not the manager of their own medication.

Guanylin and uroguanylin stimulate lipolysis in human visceral adipocytes.

BACKGROUND/OBJECTIVES: Uroguanylin and guanylin are secreted by intestinal epithelial cells as prohormones postprandially and act on the hypothalamus to induce satiety. The impact of obesity and obesity-associated type 2 diabetes (T2D) on proguanylin and prouroguanylin expression/secretion as well as the potential role of guanylin and uroguanylin in the control of lipolysis in humans was evaluated. SUBJECTS/METHODS: Circulating and gastrointestinal expression of proguanylin (GUCA2A) and prouroguanylin (GUCA2B) were measured in 134 subjects. In addition, plasma proguanylin and prouroguanylin were measured before and after weight loss achieved either by Roux-en-Y gastric bypass (RYGB) (n=24) or after a conventional diet (n=15). The effect of guanylin and uroguanylin (1-100 nmol l(-1)) on lipolysis was determined in vitro in omental adipocytes. RESULTS: Circulating concentrations of prouroguanylin, but not proguanylin, were decreased in obesity in relation to adiposity. Weight loss achieved by RYGB increased plasma proguanylin and prouroguanylin. Obese T2D individuals showed higher expression of intestinal GUCA2A as well as of the receptors of the guanylin system, GUCY2C and GUCY2D, in omental adipocytes. The incubation with guanylin and uroguanylin significantly stimulated lipolysis in differentiated omental adipocytes, as evidenced by hormone-sensitive lipase phosphorylation at Ser563, an increase in fatty acids and glycerol release together with an upregulation of several lipolysis-related genes, including AQP3, AQP7, FATP1 or CD36. CONCLUSIONS: Both guanylin and uroguanylin trigger lipolysis in human visceral adipocytes. Given the lipolytic action of the guanylin system on visceral adipocytes, the herein reported decrease of circulating prouroguanylin concentrations in obese patients may have a role in excessive fat accumulation in obesity.

Differential expression of interleukin-17 and interleukin-22 in inflamed and non-inflamed synovium from osteoarthritis patients.

OBJECTIVE: Synovitis associated with osteoarthritis (OA) is directly responsible for several clinical symptoms and reflects OA's structural progression. This study sought to analyze the expression of proinflammatory mediations, including Interleukin (IL)-17 and IL-22, which play key roles in regulating inflammatory processes, in inflamed and non-inflamed areas of osteoarthritic synovium. METHODS: Synovium from knees of 32 OA patients were collected at surgery. Macroscopic evaluation of inflammation enabled inflamed and non-inflamed areas to be separated. Samples were incubated to obtain tissue-conditioned media. Quantitative mRNA expression of proinflammatory mediators was analyzed by RT-PCR and protein levels by ELISA and gelatin zymography. Immunohistochemistry and histology were performed. RESULTS: Inflamed synovium were characterized by increased leukocyte infiltration and a higher vessel-to-tissue area ratio than non-inflamed tissues. Macrophages, T and B lymphocytes, and some neutrophils were found only in the inflamed tissue, and only in the subintimal layer. Levels of proinflammatory cytokines and MMP-9 were significantly higher in tissue-conditioned media from inflamed than non-inflamed tissues. Inflamed areas were associated with higher expression of IL-17 and IL-22, both correlated with the combined release of IL-6, IL-23, and TGFß1. CONCLUSION: Our results showed that inflammatory cytokines, including IL-17 and IL-22, are expressed at higher levels by inflamed OA synovium and suggest IL-22 involvement in OA pathophysiology. This study will help identify new therapeutic strategies for OA, especially the targeting of IL-22 to decrease inflammation.

Leptin administration activates irisin-induced myogenesis via nitric oxide-dependent mechanisms, but reduces its effect on subcutaneous fat browning in mice.

UNLABELLED: BACKGROUND/OBJETIVES: Obese leptin-deficient ob/ob mice exhibit high adiposity and reduced muscle mass with leptin replacement promoting weight loss and inducing muscle accretion through PGC-1α-dependent mechanisms. Our aim was to analyze in vivo and in vitro the effect of leptin on FNDC5, a novel PGC-1α-dependent myokine that is synthesized and cleaved to form irisin that induces white adipose browning. METHODS/RESULTS: Twelve-week-old male wild-type and ob/ob mice were divided in three groups as follows: control, leptin-treated (1 mg kg(-1) day(-1)) and pair-fed. Leptin administration was associated with increased gastrocnemius weight and cell surface area, higher Pgc1a and Fndc5 transcript levels and a slight increase in circulating irisin. Leptin upregulated Fndc5 expression through nitric oxide (NO)-dependent mechanisms in murine C2C12 myocytes and stimulated both basal and irisin-stimulated myogenesis, as evidenced by increased myocyte cell proliferation, higher myogenin and myonectin transcript levels together with lower mRNA expression of myostatin and dystrophin and the muscle atrophy-related factors MuRF1 and MAFbx. Interestingly, leptin downregulated Fndc5 expression in a NO-independent manner in murine differentiated subcutaneous adipocytes. Furthermore, leptin prevented the irisin-induced upregulation of both brown (Ucp1 and Cidec) and beige (Tmem26) adipocyte-specific genes and the increase in uncoupling protein-1-positive cells. CONCLUSIONS: Taken together, our results provide evidence for a regulatory role of leptin on FNDC5/irisin, favoring muscle accretion but reducing fat browning.

Prevalencia de patología cardíaca en la enfermedad de Chagas: años 2004-2012. Programa y Red de Chagas de CABA / Prevalence of cardiac pathology in Chagas disease: 2004 -2012. Program and Chagas CABA network

El Instituto Universitario de Ciencias de las Salud ha mostrado un particular compromiso con la formación de sus estudiantes en la estrategia de Atención Primaria de la Salud, con las prácticas asistenciales dedicadas al 1er nivel de atención ambulatoria y a las patologías prevalentes en ese ámbito. Del mismo modo se han desenvuelto las actividades de formación en investigación. Como exponente de esa orientación, la revista Ciencias de la Salud publicó en el Vol. 2, N°1, 2011:4-9, el artículo “Prevalencia de la Enfermedad de Chagas” de Érica G. Morais, que había obtenido el premio “Futuros Líderes”, otorgado por el Curso Anual Internacional de Investigación en Ciencias de la Salud (IUCS-AMA, Prof. Carlos Álvarez Bermúdez). Aquella investigación formaba parte de un proyecto más amplio realizado en el Hospital Teodoro Álvarez entre 2004 y 2012, en el que participaron un conjunto de investigadores, que compartieron la autoría de la actual publicación. El Dr. Jorge Mitelman, Prosecretario de Ciencia y Técnica del IUCS e integrante de ese equipo, preparó además una reseña sobre la jornada del INCOSUR, realizada en abril del presente año, describiendo asimismo el proceso de desarrollo de la Ciudad de Buenos Aires, como área no endémica, para encarar las consecuencias de la enfermedad de Chagas

Allergic reaction to undeclared lupin in a chocolate

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Reduced hepatic aquaporin-9 and glycerol permeability are related to insulin resistance in non-alcoholic fatty liver disease.

BACKGROUND/OBJECTIVES: Glycerol represents an important metabolite for the control of lipid accumulation and hepatic gluconeogenesis. We investigated whether hepatic expression and functionality of aquaporin-9 (AQP9), a channel mediating glycerol influx into hepatocytes, is impaired in non-alcoholic fatty liver disease (NAFLD) and steatohepatitis (NASH) in the context of insulin resistance. SUBJECTS/METHODS: Liver biopsies were obtained from 66 morbid obese patients undergoing bariatric surgery (66% women, mean body mass index (BMI) 46.1±1.0 kg m(-2)) with available liver echography and pathology analysis of the biopsies in this cross-sectional study. Subjects were classified according to normoglycemia (NG), impaired glucose tolerance (IGT) or type 2 diabetes (T2D). Hepatic expression of AQP9 was analyzed by real-time PCR, western blotting and immunohistochemistry, while glycerol permeability (P(gly)) was measured by stopped-flow light scattering. RESULTS: AQP9 was the most abundantly (P<0.0001) expressed aquaglyceroporin in human liver (AQP9>>>AQP3>AQP7>AQP10). Obese patients with T2D showed increased plasma glycerol as well as lower P(gly) and hepatic AQP9 expression. The prevalence of NAFLD and NASH in T2D patients was 100 and 65%, respectively. Interestingly, AQP9 expression was decreased in patients with NAFLD and NASH as compared with those without hepatosteatosis, in direct relation to the degree of steatosis and lobular inflammation, being further reduced in insulin-resistant individuals. The association of AQP9 with insulin sensitivity was independent of BMI and age. Consistent with these data, fasting insulin and C-reactive protein contributed independently to 33.1% of the hepatic AQP9 mRNA expression variance after controlling for the effects of age and BMI. CONCLUSIONS: AQP9 downregulation together with the subsequent reduction in hepatic glycerol permeability in insulin-resistant states emerges as a compensatory mechanism whereby the liver counteracts further triacylglycerol accumulation within its parenchyma as well as reduces hepatic gluconeogenesis in patients with NAFLD.