25 research outputs found

    Dietary Supplementation with Omega-3-PUFA-Rich Fish Oil Reduces Signs of Food Allergy in Ovalbumin-Sensitized Mice

    Get PDF
    We investigated the effect of dietary supplementation with n-3 PUFA (fish oil source) in an experimental model of food allergy. Mice were sensitized (allergic group) or not (nonallergic group) with OVA and were fed with OVA diet to induce allergy signals. Mice were fed with regular diet in which 7% of lipid content was provided by soybean (5% of n-3 PUFA) or fish (25% of n-3 PUFA) oil. Allergic group mice had increased serum levels of antiovalbumin IgE and IgG1 and changes in small intestine, characterized by an increased edema, number of rolling leukocytes in microcirculation, eosinophil infiltration, mucus production, and Paneth cell degranulation, in comparison to non-allergic group. All these inflammatory parameters were reduced in mice fed high-n-3-PUFA diet. Our data together suggest that diet supplementation with n-3 PUFA from fish oil may consist of a valid adjuvant in food allergy treatment

    VALIDAÇÃO DA SÍNDROME METABÓLICA E DE SEUS COMPONENTES AUTODECLARADOS NO ESTUDO CUME

    Get PDF
    RESUMO O objetivo deste estudo foi analisar a validade dos diagnósticos autodeclarados de síndrome metabólica (SM) e de seus componentes pelos participantes da Coorte de Universidades Mineiras (CUME). Uma subamostra de 172 participantes da coorte (33 homens e 139 mulheres, idade 38 ± 11 anos) foi aleatoriamente selecionada para este estudo. A presença de SM foi definida segundo os critérios da International Diabetes Federation (IDF). Dados de peso, altura, pressão arterial, concentração sérica de glicose, triglicerídeos e HDL-c foram autodeclarados em questionário online da coorte e as mesmas variáveis foram aferidas presencialmente mediante protocolo padronizado em laboratórios das instituições de ensino superior envolvidas no projeto. Os dados autodeclarados e aferidos foram comparados por meio de coeficiente de correlação intraclasse (CCI), coeficiente Kappa (k) e diferenças entre medidas autodeclaradas e aferidas segundo a metodologia de Bland e Altman. As prevalências da SM foram de 4,7%e 5,2%, de acordo com os dados autodeclarados e aferidos, respectivamente. O coeficiente Kappa entre diagnósticos de SM autodeclarado e aferido foi 0,814, indicando concordância quase perfeita, situação similar à observada para a obesidade (k=0,882). Os demais componentes da SM apresentaram concordâncias moderadas (k=0,41 a 0,60). Os CCIs também indicaram excelente concordância para peso, estatura, IMC e HDL-c, respectivamente, 0,989, 0,995, 0,983 e 0,761. A glicose apresentou baixa concordância (CCI: 0,336). Concluiu-se que participantes do projeto CUME forneceram informações válidas para os diagnósticos autodeclarados de SM e de seus componentes

    High resting energy expenditure in women with episodic migraine: exploring the use of predictive formulas

    Get PDF
    IntroductionMigraine is a common and disabling primary headache, and its pathophysiology is not fully understood. Previous studies have suggested that pain can increase humans’ Resting Energy Expenditure (REE). However, no previous study has investigated whether the REE of individuals with migraine differs from the general population. Therefore, this study aims to assess whether the REE of women with migraine differs from that of women without headaches. We also tested the accuracy of REE predictive formulas in the migraine patients.MethodsThis cross-sectional study involves 131 adult women aged between 18 and 65 years, 83 with migraine and 48 without (controls). We collected clinical, demographic, and anthropometric data. Migraine severity was measured using the Migraine Disability Test and Headache Impact Test, version 6. The REE was measured by indirect calorimetry, and it was compared with the predicted REE calculated by formulas.ResultsPatients with migraine had higher REE when compared to controls (p < 0.01). There was a positive correlation between REE and the patient-reported number of migraine attacks per month (Rho = 0.226; p = 0.044). Mifflin-St Jeor and Henry and Rees were the predictive formulas that have more accuracy in predicting REE in women with migraine.DiscussionConsidering the benefits of nutritional interventions on treating migraines, accurately measuring REE can positively impact migraine patient care. This study enhances our understanding of the relationship between pain and energy expenditure. Our results also provide valuable insights for healthcare professionals in selecting the most effective predictive formula to calculate energy expenditure in patients with migraine

    Dysbiotic oral microbiota contributes to alveolar bone loss associated with obesity in mice

    Get PDF
    Periodontal diseases (PD) are inflammatory conditions that affect the teeth supporting tissues. Increased body fat tissues may contribute to activation of the systemic inflammatory response, leading to comorbidities. Some studies have shown that individuals with obesity present higher incidence of PD than eutrophics. Objective: To investigate the impact of obesity on periodontal tissues and oral microbiota in mice. Methodology: Two obesity mice models were performed, one using 12 weeks of the dietary protocol with a high-fat (HF) diet in C57BL/6 mice and the other using leptin receptor-deficient mice (db/db-/-), which became spontaneously obese. After euthanasia, a DNA-DNA hybridization technique was employed to evaluate the microbiota composition and topical application of chlorhexidine (CHX), an antiseptic, was used to investigate the impact of the oral microbiota on the alveolar bone regarding obesity. Results: Increased adipose tissue may induce alveolar bone loss, neutrophil recruitment, and changes in the oral biofilm, similar to that observed in an experimental model of PD. Topical application of CHX impaired bone changes. Conclusion: Obesity may induce changes in the oral microbiota and neutrophil recruitment, which are associated with alveolar bone loss

    Efeito do fenofibrato sobre o metabolismo de ratos com ousem indução de esteatose hepática

    No full text
    Exportado OPUSMade available in DSpace on 2019-08-14T14:00:10Z (GMT). No. of bitstreams: 1 tese_adaliene_1_.pdf: 1848576 bytes, checksum: 944a3b600ad2f9a6ef9f5baa4b217790 (MD5) Previous issue date: 8Este trabalho teve por finalidade estudar os efeitos do fenofibrato, ativador do PPARá (receptor nuclear ativado pelos proliferadores de peroxissomos-á) e da esteatose hepática, induzida pela administração dietética de ácido orótico, sobre o metabolismo do tecido adiposo (TA) e fígado de ratos. Ratos Wistar machos foram divididos em 4 grupos experimentais: 1) alimentados com dieta balanceada (C); 2) Alimentados com dieta balanceada adicionada de 100 mg.Kg-1PC.dia-1 de fenofibrato (C+F) 3) alimentados com a dieta C suplementada com 1% de ácido orótico (AO); 4) alimentados com dieta balanceada contendo 1% de AO adicionado de 100 mg.Kg-1PC.dia-1 de fenofibrato (AO+F). Os animais foram alimentados por um período de 9 dias.O tratamento com fenofibrato reduziu o ganho de peso corporal, a adiposidade, a concentração plasmática de triacilglicerol (TAG) e de colesterol total mas não influenciou a ingestão alimentar e as concentrações plasmáticas de leptina, glicose, glicerol, ácidos graxos einsulina quando comparado aos animais controles. A atividade da enzima lípase lipoprotéica (LPL) do TA epididimal apresentou-se diminuída nos animais tratados com fenofibrato em relação aos controles. Além disso, pode ser verificada uma redução de 34 % na lipogênese de novo do tecido adiposo induzida pelo tratamento com fenofibrato quando comparada aos controles. A captação de glicose por adipócitos foi avaliada a partir da incubação dessas células com 2- deoxi [3H]glicose (2-DG), e os resultados mostraram que o tratamento com fenofibrato aumentou a captação de glicose tanto no estado basal quanto estimulada pela insulina por adipócitos quando comprada ao controle. Esse efeito não foi devido ao aumento no conteúdo da proteína GLUT-4 (transportador de glicose) no TA. Os resultados também demonstraram que o fenofibrato aumentou a expressão do mRNA da enzima acil CoA oxidase (ACO) e do PPARá no fígado e da enzima carnitina palmitoil transferase1 (CPT-1) e ACO no TA em relação aos controles. A administração dietética de AO aos animais durante 9 dias induziu um aumento Resumo ii significante no conteúdo hepático de gordura total (160%) e redução na concentração plasmática de TAG (30%) e colesterol total (28%) comparado aos controles. A dministraçãode fenofibrato aos animais alimentados também com AO (AO+F) impediu o acúmulo de gordura hepática e reduziu a concentração plasmática de TAG (50%) e colesterol (46%) em relação ao grupo não tratado com fenofibrato(AO). Consistentemente, a análise histológica dofígado dos animais AO mostrou um acentuado acúmulo de gordura ao passo que o tratamento com fenofibrato nesses animais impediu o desenvolvimento da esteatose. O tratamento com AO não alterou a lipogênese de novo, entretanto, a administração de fenofibrato diminuiu as taxas lipogênicas no tecido adiposo dos animais AO+F. Os resultados mostraram um aumento de 40% na atividade da enzima LPL do tecido adiposo dos animais AO comparado aos controles ao passo que o tratamento com fenofibrato (OA+F) reduziu em 50% a atividadedessa enzima em relação ao grupo AO. A suplementação com AO aumentou a captação de glicose no estado basal e estimulado com insulina por adipócitos em relação ao C. Esse efeito foi devido, pelo menos em parte, ao aumento no conteúdo da proteína GLUT-4 no TA dos animais AO. O tratamento com fenofibrato (OA+F) não alterou a captação basal ou estimulada pela insulina por adipócitos comparado ao grupo AO. A expressão hepática do mRNA para o PPARá e a enzima ACO foram 85% e 68% reduzidas nos animais AO comparada aos controles, respectivamente. O tratamento com fenofibrato (OA+F) aumentou a expressão hepática do PPARá e da enzima ACO ao passo que a expressão da CPT-1 não foi alterada quando comparado ao grupo não tratado, AO. Em resumo, esse trabalho fornece evidências de que o fenofibrato impede o desenvolvimento da esteatose hepática induzida pela administração dietética de AO através do aumento no catabolismo hepático de lipídios. Esse efeito é provavelmente mediado peloPPARá, principalmente através da indução da expressão da enzima alvo ACO envolvida no metabolismo de lipídios. Embora os compartimentos mitocondriais e peroxissomais contribuam para a oxidação dos AG, nossos dados não apontam a mitocôndria como um sítio Resumoiii importante para a oxidação de lipídios induzida pelo tratamento com fenofibrato. Além dos efeitos no fígado, o fenofibrato tem influência relevante no metabolismo do tecido adiposo que contribui, por sua vez, para a redução da adiposidade, a qual parece ser conseqüente aoaumento da oxidação local de ácidos graxos, e melhora da captação celular de glicose.The experiments reported here were designed to study the effect of fenofibrate (stimulant of peroxisome proliferator-activated receptor á - PPARá) and hepatic steatosis induced by orotic acid administration on the metabolism of adipose tissue and liver. Wistar male rats were divided into 4 experimental groups: 1) fed a balanced diet (C); 2) fed a balanced diet plus 100 mg.Kg-1bw.day-1 fenofibrate (C+F) 3) fed a balanced dietsupplemented with 1% orotic acid (OA); 4) fed C diet containing 1% OA plus 100 mg.Kg-1 bw.day-1 fenofibrate (OA+F), which were fed during 9 days. Fenofibrate lowered body weight gain and adiposity, plasma triglyceride and total cholesterol but had no influence on food intake, plasma leptin, glucose, glycerol, free fatty acid (FFA) and insulin levels when compared to control animals. The activity of lipoprotein lípase (LPL) of treated animals decreased 50 % in epididymal adipose tissue. In this study, we have shown a 34 % decrease of epididymal adipose tissue de novo lipogenesis by fenofibrate compared to C. The glucose uptake was also evaluated by adipocyte incubation with deoxyglucose (2-DG). Fenofibrate treatment increased the glucose uptake in basal or insulinstimulated adipocytes when compared to C. This effect was not due to increased GLUT-4 protein content on adipose tissue. The results also demonstrate that fenofibrate increased the mRNA expression of ACO and PPARá in the liver and CPT-1and ACO in the adipose tissuewhen compared to control animals. The administration of OA to rats for 9 days induced significant increase in total fat liver content (160%) and decreases in plasma TG concentration (30%) and total cholesterol(28%) compared to control animals. Fenofibrate administration to rats fed OA (OA+F) prevented fat liver induction and reduced the plasma triglyceride (50%), and cholesterol (46%) concentrations in relation to the not treated group (OA). Consistently, histological examination of the liver from OA rats showed marked lipid accumulation whereas the treatment with fenofibrate in these animals prevented the development of fat liver. OA Abstract v treatment did not change de novo lipogenesis, however, fenofibrate administration caused a 40% decrease in the lipogenic rates in adipose tissue from OA+F treated rats. The results showed 40% increase in LPL activity in epididymal adipose tissue from OA treated rats when compared to C group while the fenofibrate treatment (OA+F) reduced in 50% the LPL activity in relation to OA group. OA administration enhanced the adipocyte glucose uptake in basal or insulin-stimulated conditions compared to control group. This effect was due, at leastin part, to an increase in the adipose tissue GLUT-4 protein content of OA treated rats. The fenofibrate treatment (OA+F) did not change the glucose uptake in basal or stimulated adipocyte when compared to OA animals. The liver mRNA expression of PPARá and ACO were 85% and 68% decreased in OA treated group when compared to control group,respectively. The fenofibrate treatment (OA+F) increased the liver PPARá and ACO expression whereas the CPT-1 expression was not altered when compared to the not treated group OA.In summary, we provide evidence that fenofibrate decreases the hepatic steatosis induced by orotic acid administration through enhancement of lipid catabolism in rat liver. This effect is probably mediated by PPARá, mainly through the induction of the target enzyme ACO involved in hepatic lipid metabolism. Although both the peroxisomal and the mitochondrial compartments contribute to increased oxidation of fatty acids, our data did not support a role of mitochondria in wasting energy, which is instead an intrinsic property of peroxisomal â-oxidation. Besides its effects on liver, fenofibrate seems to play a relevant role on the metabolism of adipose tissue which may contribute to decrease adiposity, probably as a result of the local increased fatty acid oxidation in the tissue, and improve the Glucose uptake by adipocyte

    Consumption of baru nuts (Dipteryx alata) in the treatment of obese mice

    No full text
    ABSTRACT: The present study evaluated the effects of baru nut consumption on body weight, percent adiposity, amount of adipose tissue and blood levels in obese male Swiss mice. After inducing obesity by providing high-glucose diet (60 days), the mice were divided into 4 groups (7 animals per group) and were fed on a control diet (C), high-glucose diet (HG) or high-glucose diet added with baru (HGBA) or soybean oil (HGSO). Groups fed with diet HGBA had a decrease in the weight gain and glucose and triglyceride levels when compared to diet HG. Aimals fed with HG exhibited a higher proportion of epididymal and retroperitoneal adipose tissue. The inclusion of baru nut in the diet improved the control of weight gain and glucose and triglyceride levels in obese mice

    Valida??o da s?ndrome metab?lica e de seus componentes autodeclarados no estudo CUME.

    No full text
    The aim of this study was to analyze the validity of self-reported diagnoses of metabolic syndrome (MetS) and its components through participants of the Cohort of Universities of Minas Gerais (CUME). A subsample of 172 cohort participants (33 males and 139 females, age 38 ? 11 years) was randomly selected for this study. The presence of MetS was defined according to the criteria of the International Diabetes Federation (IDF). Data on weight, height, blood pressure, and serum concentration of glucose, triglycerides and HDL-c were self reported in an online cohort questionnaire, and the same variables were measured using a standardized protocol in laboratories of higher education institutions involved in the project. Self-reported and measured data were compared by means of intraclass correlation coefficient (ICC), Kappa coefficient (k) and differences between self-reported and measured data, according to the Bland and Altman method. The prevalence of MetS was 4.7% and 5.2% according to self-reported and measured data, respectively. The Kappa coefficient between diagnoses of self-reported and measured MetS was 0.814, indicating almost perfect agreement, a situation similar to that observed for obesity (k = 0.882). The other components of MetS had moderate agreement (k = 0.41 to 0.60). The ICC also indicated excellent agreement for weight, height, BMI and HDL-c, respectively, 0.989, 0.995, 0.983 and 0.761. Glucose presented low agreement (ICC: 0.366). The study concludes that the CUME project participants provided valid information for the self-reported diagnoses of MetS and its components.O objetivo deste estudo foi analisar a validade dos diagn?sticos autodeclarados de s?ndrome metab?lica (SM) e de seus componentes pelos participantes da Coorte de Universidades Mineiras (CUME). Uma subamostra de 172 participantes da coorte (33 homens e 139 mulheres, idade 38 ? 11 anos) foi aleatoriamente selecionada para este estudo. A presen?a de SM foi definida segundo os crit?rios da International Diabetes Federation (IDF). Dados de peso, altura, press?o arterial, concentra??o s?rica de glicose, triglicer?deos e HDL-c foram autodeclarados em question?rio online da coorte e as mesmas vari?veis foram aferidas presencialmente mediante protocolo padronizado em laborat?rios das institui??es de ensino superior envolvidas no projeto. Os dados autodeclarados e aferidos foram comparados por meio de coeficiente de correla??o intraclasse (CCI), coeficiente Kappa (k) e diferen?as entre medidas autodeclaradas e aferidas segundo a metodologia de Bland e Altman. As preval?ncias da SM foram de 4,7%e 5,2%, de acordo com os dados autodeclarados e aferidos, respectivamente. O coeficiente Kappa entre diagn?sticos de SM autodeclarado e aferido foi 0,814, indicando concord?ncia quase perfeita, situa??o similar ? observada para a obesidade (k=0,882). Os demais componentes da SM apresentaram concord?ncias moderadas (k=0,41 a 0,60). Os CCIs tamb?m indicaram excelente concord?ncia para peso, estatura, IMC e HDL-c, respectivamente, 0,989, 0,995, 0,983 e 0,761. A glicose apresentou baixa concord?ncia (CCI: 0,336). Concluiu-se que participantes do projeto CUME forneceram informa??es v?lidas para os diagn?sticos autodeclarados de SM e de seus componentes
    corecore