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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
231

The Role of Inflammation in Diet-Induced Insulin Resistance

Alexander, Lindsey Ann January 2009 (has links)
No description available.
232

Akuta glykemiska episoders påverkan på vardagen för insulinbehandlade personer med diabetes : En kvalitativ litteraturstudie / Acute glycemic episodes and their impact on everyday life amongst those with insulin-treated diabetes : A qualitative literature review

Tallroth, Johannes, Kristiansson, Max January 2024 (has links)
Bakgrund: Diabetes är ett samlingsnamn för en grupp metabola sjukdomar med den gemensamma nämnaren att kroppen har en oförmåga att producera eller ta upp insulin Diabetes medför, bland annat, en risk för akuta glykemiska episoder relaterat till kroppens oförmåga att vidmakthålla en normal blodglukosnivå. Syfte: Att sammanställa kunskap om hur personer med insulinbehandlad diabetes upplever att medvetenheten om akuta glykemiska episoder påverkar det dagliga livet. Metod: En kvalitativ litteraturstudie baserad på elva vetenskapliga primärstudier inhämtade från databaserna PubMed respektive CINAHL. Resultat: Tre kategorier och sex underkategorier genererades; ”En förändrad vardag” med underkategorierna; ”Planera eller ge upp”, ”Ett behov av andras stöd” samt ”Ofrånkomliga utmaningar”, ”Att leva med oro” med underkategorierna; ”Varierande syn på lämplig blodglukosnivå”, ”Självkritik och skam” samt ”Rädsla för liv och hälsa” och ”Varierande strategier i vardagen” utan underkategorier. Slutsats: Personer med insulinbehandlad diabetes möter en mängd utmaningar i vardagen relaterat till medvetenhet om akuta glykemiska episoder. Utmaningarna inkluderar särskilda krav på minutiös planering och inte sällan förändringar i vardagen. Förändringar i vardagslivet kräver i de flesta fall implementering av nya strategier för att kunna hantera de utmaningar diabetessjukdomen medför. Utmaningarna är inte enbart av praktisk natur utan även av en mer psykosocial natur som leder till att många upplever att stigmatisering från omgivningen och orealistiska krav på sig själva resulterar i ohälsosam självkritik och ibland skam relaterat till de akuta glykemiska episoder de ofrånkomligen drabbas av i olika utsträckning. / Background: Diabetes is a collective name for a group of metabolic diseases with the denominator that the body experience an inability to produce, or absorb, insulin in sufficient quantities. Diabetes entails, amongst other potential problems, a non-unsubstantiated risk of acute glycemic episodes due to the body´s inadequate ability to maintain a normal blood glucose level. Aim: To compile knowledge on how persons suffering from insulin treated diabetes manage the awareness of the threat that acute glycemic episodes impose on everyday life. Method: A qualitative study based on eleven primary scientific studies that was obtained from the databases PubMed and CINAHL. Result: Three categories and six sub-categories emerged; “A change in everyday life” containing the sub-categories “plan or give up”, “A need for others” and “Unavoidable changes” “Living with worry” containing the sub-categories “Different views on blood glucose levels”, Self-criticism and shame” and “Fear for life and health” and lastly “Various strategies in day-to-day life” which was without sub-categories. Conclusion: People with insulin treated diabetes faces a variety of challenges in everyday life related to acute glycemic episodes. The variety of challenges include special requirements when it comes to planning and scheduling everyday life. Changes in everyday life often requires the implementation of new strategies to handle the challenges imposed by diabetes and it´s symptoms. Challenges which are not only practical in nature but also entails a more psychosocial aspect that can lead to feelings of stigmatization and unrealistic demands on one self. Feelings that can result in unhealthy self-criticism, and sometimes shame, related to the symptoms of inevitable acute glycemic episodes.
233

Neuropsychologische, psychiatrische und metabolische Konsequenzen des Gestationsdiabetes / eine Verlaufsbeobachtung 5 Jahre post partum

Hardenberg, Tatjana von 21 February 2006 (has links)
Worauf schon die Literatur hinweist, kann mit dieser Studie bestätigt werden: Eine langfristige metabolische Kontrolle stellt einen essentiellen Faktor in der adäquaten Betreuung von GDM Patientinnen dar. Dies wird nicht nur durch eine IGT bei einem Drittel der Probandinnen, sondern auch durch durchschnittlich höhere Insulin- und Kortisolspiegel 5,5 Jahre nach der Erkrankung bestätigt. Die Objektivierung einer psychiatrischen Beeinträchtigung oder Einschränkung neuropsychologischer Funktionen aufgrund einer persistierenden Hyperglykämie konnte nicht eindeutig bestätigt werden. In Gedächtnistests sowie im subjektiven psychischen und somatischen Befinden konnten nur tendenzielle Unterschiede gemessen werden. Dies gilt auch in Abhängigkeit von der metabolischen Kontrolle unabängig eines zu Grunde liegenden Gestationsdiabetes. Auch wenn die Studie keine kognitive Beeinträchtigung nachweisen konnte, sind Störungen durch langfristige metabolische Dysfunktionen nicht auszuschliessen. Bei der Durchführung weiterer derartiger Studien sind unbedingt die von uns einbezogenen Stoffwechselparameter (Kortisol, Insulin und Glukose) mit Einfluss auf die Kognition einzubeziehen. Ein regelmässiges Follow-Up der Schwangeren mit Gestationsdiabetes sollte in jedem Fall erfolgen, um einen postpartalen Typ-2-Diabetes mellitus rechtzeitig zu erkennen und therapieren zu können. / This study can confirm the importance of long term metabolic control in GDM Patients as the existing literature is already pointing out. It is an essential aspect in the adequate support of patients with gestational diabetes. It is shown not only by an impaired glucose tolerance in one third of GDM Patients but also by insuline and glucagon levels above average 5.5 Years after the concerning pregnancy. The objectification of psychiatric impairment or impairment in neuropsychological functions due to persistent hyperglycaemia could not be proved clearly. In memory tests as in psychological or somatic findings we could only measure tendencies without significant differences. This counts also for the metabolic control itself without the existence of preceding gestational diabetes. Even though there were no cognitive impairments proven, we could not exclude any disturbances due to long term metabolic dysfunction. With the execution of future studies, metabolic parameter that we used (Insulin, Glucagone, Glucose) should be included as influencing parameter to cognitive functions. A Follow Up in GDM Patients should be performed regularly in any case, not only to exclude the development of a possible diabetes mellitus.
234

Le rôle du récepteur B1 des kinines dans l'insulite et dans les complications du diabète de type 1 dans un modèle de choc spectique

Tidjane, Nejla 04 1900 (has links)
Les kinines sont des peptides vasoactifs et des neuromédiateurs centraux impliqués dans le contrôle cardiovasculaire, la douleur et l’inflammation. Leurs actions sont relayées par deux types de récepteurs couplés aux protéines G : le récepteur B2 (RB2), constitutif, et le récepteur B1 (RB1), inductible en présence de lésions tissulaires, de cytokines pro-inflammatoires, d’endotoxines bactériennes et dans certaines pathologies tel que le diabète. Le diabète sucré augmente à l’échelle mondiale et son étiologie est complexe; il aggrave les infections sévères et augmente la mortalité par hyperbactériémie résistante à un contrôle thérapeutique et une prise en charge en soins intensifs. Les décès surviennent dans la grande majorité des cas à la suite de l'apparition d'une coagulation intra- vasculaire disséminée (CIVD). Ce projet a pour but d’étudier le rôle du RB1 dans la CIVD dans un modèle de diabète de type 1 induit par la streptozotocine (STZ) (Article 1) et dans l’insulite (Article 2). La CIVD est produite par l’injection de lipopolysaccharide (LPS, 2 mg/kg, i.p.), 4 jours après le traitement à la STZ (65 mg/kg, i.p.). Dans le premier article, nous avons montré une augmentation significative de l'œdème et de la perméabilité vasculaire par le bleu d’Évans dans le rein, le poumon, le coeur et le foie chez les rats traités au LPS et/ou à la STZ, une situation qui favorise une hémoconcentration et le développement d'un état d'hypercoagulabilité. Nous avons aussi montré la présence d'indices de thrombus et de lésions tissulaires dans l'étude histologique ainsi qu’une augmentation de l'expression du RB1 dans le coeur, le rein et les plaquettes sanguines. Un traitement avec l’antagoniste du RB1, le SSR240612, a corrigé l’apparition de ces anomalies et a rendu normale la glycémie chez les rats STZ et l’hyperthermie induite par le LPS. De même, le SSR240612 a nettement amélioré la survie des animaux. Les bénéfices du SSR240612 ont été reproduits par l’inhibition de la iNOS avec le 1400W et de la COX-2 avec l’acide niflumique, suggérant que les médiateurs de ces enzymes pro-inflammatoires agissent en aval du RB1.Dans le deuxième article, le rat STZ est traité du jour 4 au jour 7 avec le SSR240612 (10 mg/kg/jr per os). Cet antagoniste du RB1 bloque l’infiltration du pancréas par les macrophages et les lymphocytes TCD4+ qui sont porteurs du RB1. L’antagoniste prévient aussi l’augmentation de l’expression de la iNOS, du TNF-α, du RB1 et du TRPV1 dans le pancréas des rats diabétiques. Le traitement avec l’antagoniste du RB1 a limité la perte des cellules β des îlots de Langerhans et a corrigé l’hypoinsulinémie et l’hyperglycémie. Ces deux études mettent en lumière un rôle important du RB1 dans la létalité associée au choc septique, à la thrombose et à l’insulite. Par conséquent, le RB1 représente une cible thérapeutique prometteuse dans le traitement du diabète et de ses complications. / Kinins are vasoactive peptides and central neuromediators involved in cardiovascular control, pain and inflammation. Their effects are mediated by two G protein-coupled receptors: the constitutive B2 receptor (B2R) and the inducible B1 receptor (B1R) that is upregulated during tissue injury, in the presence of proinflammatory cytokines, bacterial endotoxins and diabetes. Diabetes has reached epidemic level and its etiology is complex. Diabetes mellitus worsens severe infections and increases mortality caused by hyperbacteremia resistant to therapeutic control and management in intensive care units. Mortality is largely secondary to the occurrence of disseminated intravascular coagulation (DIC). This project examines the role of B1R in DIC in a model of type 1 diabetes induced by streptozotocin (STZ) (Article 1) and insulitis (Article 2). DIC was induced by injection of lipopolysaccharide (LPS, 2 mg/kg i.p.) four days after treatment with STZ (65 mg/kg, i.p.). In the first article, we have shown a significant increase in edema and vascular permeability (Evans blue) in kidney, lung, heart and liver in rats treated with LPS and/or STZ, increasing the haemoconcentration and the development of hypercoagulability state. Also, we showed the presence of thrombus formation and tissue damage by histological studies, and increased expression of B1R in the heart, kidney and platelets. Treatment with the B1R antagonist, SSR240612, alleviated all those abnormalities, in addition to reducing hyperglycemia in STZ rats, LPS-induced hyperthermia and improving survival. The beneficial effects of SSR240612 were reproduced by the inhibition of iNOS with 1400W and of COX-2 with niflumic acid, suggesting that the mediators of these proinflammatory enzymes act downstream to B1R. In the second article, STZ rats were treated with SSR240612 (10 mg/kg/d, per os) from day 4 to day 7. This B1R antagonist blocked the infiltration of the pancreas by macrophages andTCD4+ lymphocytes which express B1R. The antagonist also prevented the increased expression of iNOS, TNF-α, B1R and TRPV1 in the pancreas of STZ-diabetic rats. The treatment with the B1R antagonist limited the loss of Langerhans β cells, which improved plasma insulin and normalized hyperglycemia. These studies highlight a primary role for B1R in lethality associated with septic shock, thrombosis and insulitis. Therefore, kinin B1R is a promising therapeutic target in the treatment of diabetes and its complications.
235

Estudo de variantes da leptina do receptor de leptina: impacto sobre as características relacionadas com a obesidade / Study of the leptin and the leptin receptor gene variants: impact on characteristics related with obesity

Oliveira, Raquel de 17 June 2008 (has links)
Neste estudo, foi avaliada a relação entre polimorfismos dos genes da leptina (LEP) e receptores da leptina (LEPR) e parâmetros antropométricos, leptinemia glicemia e lipídeos séricos, em indivíduos da população brasileira. Foram incluídos 238 indivíduos com idade entre 30 e 80 anos. Foram medidos o índice de massa corporal (IMC), a cintura abdominal (CA) e a razão cintura quadril (RCQ). Amostras de sangue periférico foram obtidas para análise do perfil bioquímico e extração de DNA. Os polimorfismos de nuleotideo único (SNPs) LEP G-2548A e LEPR Lys109Arg, Gln223Arg e Lys656Asn foram detectados por PCR-RFLP. Os SNPs LEPR Lys109Arg e Gln223Arg foram associados com obesidade e com IMC e CA aumentados (p<0.05). Estes polimorfismos também foram associados com leptina e glicose elevada (p<0,05). O perfil lipídico sérico foi influenciado pelo polimorfismo LEPR Lys109Arg (p<0.05). A relação entre os SNPs LEPR Lys109Arg e Gln223Arg e o perfil lipídico foi modificada pelo gênero. Os haplótipos LEP G-2548/ LEPR Lys109Arg foram relacionados com diferenças no IMC de obesos. Os haplotipos LEPR Lys109Arg/Gln223Arg foram associados com diferenças na CA e glicemia e lipídeos séricos. Em conclusão, os polimorfismos LEPR Lys109Arg e Gln223Arg estão associados com obesidade e alterações de leptina, glicose e lipídeos circulantes de forma dependente do gênero. / We have assessed the relationship between polymorphisms of the leptin (LEP) and the leptin receptor (LEPR) genes and anthropometric parameters, plasma leptin and glucose and serum lipids in individuals of the Brazilian population. We included 238 individuais with 30 to 80 years. Body mass index (BMI), abdominal circumference (AC) and waist-to-hip ratio (WHR) were measured. Peripheral blood samples were collected for analysis of the biochemical profile and DNA extraction. The single nucleotide polymorphisms (SNP) LEP G-2548A and LEPR Lys109Arg, Gln223Arg and Lys656Asn were detected by PCR-RFLP. The SNPs LEPR Lys109Arg and Gln223Arg were associated with obesity and with increased BMI and AC (p <0.05). These polymorphisms were also associated with increase leptin and glucose (p<0,05). The serum lipid profile was influenced by the LEPR Lys 1 09Arg (p<0.05). The relationship between the SNPs LEPR Lys 1 09Arg and Gln223Arg and the lipid profile was modified by gender. The haplotypes LEP G-2548A1 LEPR Lys109Arg were related with differences on BMI in obese group. The haplotypes LEPR Lys109Arg/Gln223Arg were associated with differences on AC, glucose and serum lipids. In conclusion, the LEPR Lys109Arg and Gln223Arg polymorphisms are associated with obesity and alterations in blood leptin, glucose and lipids in a gender-dependent manner.
236

Estresse oxidativo como um mecanismo dos efeitos deletérios causados pela hiperglicemia neonatal em cérebro de ratos

Rosa, Andréa Pereira January 2018 (has links)
A diabetes é um distúrbio endócrino do metabolismo dos carboidratos, clinicamente caracterizada por hiperglicemia, resultante da incapacidade do organismo em secretar insulina, defeitos na sua ação ou ambos. Na última década, houve um crescente aumento no número de trabalhos sobre a múltipla hereditariedade de um tipo de diabetes rara e não imunológica diagnosticada antes dos 6 meses de vida, a diabetes neonatal (DN). A maioria dos estudos, existentes na literatura referentes à DN, foi realizada em pacientes e aborda principalmente aspectos clínicos, etiológicos e terapêuticos. No entanto, existe uma deficiência de estudos realizados em modelos animais, a fim de avaliar danos moleculares em tecidos submetidos à hiperglicemia neonatal. Recentemente, as consequências da diabetes no sistema nervoso central (SNC) têm recebido maior atenção, uma vez que os recentes estudos mostram que a hiperglicemia é capaz de promover a ruptura da homeostase redox no cérebro de ratos. Neste sentido, o estresse oxidativo (EO) parece representar um dos mecanismos pelos quais a hiperglicemia danifica o tecido cerebral em um período crucial de desenvolvimento. Diante disso, o presente trabalho objetivou estudar não só a relação do EO com a hiperglicemia neonatal em cérebro de ratos, mas também avaliar se os danos oxidativos promovidos pelas espécies reativas de oxigênio (ERO) na condição hiperglicêmica podem estar envolvidos no processo de morte celular neuronal. Para isso, foram utilizados ratos Wistar de 5 dias de vida, divididos em dois grupos: controle e diabético. O modelo de diabetes foi induzido pela administração intraperitoneal de estreptozotocina (STZ) em uma única dose de 100 mg/Kg peso corporal, sendo que foram considerados diabéticos os ratos com glicemia >200mg/dL. Os animais foram sacrificados com 10 dias de vida, ou seja, 5 dias após a administração de STZ. O cérebro total dos animais foi homogeneizado, centrifugado e o homogeneizado utilizado para as medidas de parâmetros de EO e expressão proteica. Além disso, o cérebro total foi utilizado em cortes histológicos para análise do parâmetro de morte celular neuronal, avaliada pela técnica FluoroJade C. Os parâmetros de EO analisados foram o metabolismo da glutationa, que engloba a atividade das enzimas glutationa S-transferase (GST), glutationa redutase (GR), glutamato-cisteína ligase (GCL) e a 8 determinação da concentração de glutationa total e reduzida (GSH/GSSG). A medida do peróxido de hidrogênio (H2O2) também foi avaliada, juntamente com a quantificação proteica por “Western Blot” do fator nuclear eritroide relacionado ao fator 2 (Nrf2), da superóxido dismutase (SOD), da catalase (CAT), da glutationa peroxidase (GPx), da heme oxigenase 1 (HO-1) e da tiorredoxina (TRX). Os parâmetros relativos à sobrevivência e morte celular avaliados foram a quantificação proteica por “Western Blot” da proteína cinase B (AKT), da proteína cinase B fosforilada (p-AKT), da glicogênio sintase cinase 3 β (GSK3β), da p38 proteína cinase ativada por mitógenos (p38), proteína cinase c-Jun N-terminal (JNK), da célula-B de linfoma 2 (Bcl2) e da proteína X associada a Bcl2 (Bax). Os ratos submetidos ao modelo de hiperglicemia neonatal não apresentaram diferenças significativas nos parâmetros relacionados ao metabolismo da glutationa (GST, GR, GCL e GSH/GSSG), tampouco nas concentrações de H2O2 quando comparados ao grupo controle. A expressão proteica do Nrf2 foi diminuída no grupo diabético, enquanto que a expressão da CAT, HO-1 e TRX se apresentaram aumentadas no grupo diabético quando comparado ao grupo controle. Não foram encontradas diferenças significativas nas expressões proteicas da SOD e GPx. As expressões proteicas das proteínas p38 e Bcl2 foram aumentadas, enquanto a expressão da p-AKT se mostrou reduzida no grupo diabético. Já com relação à expressão das proteínas JNK, GSK3β e Bax não houve diferença significativa nos grupos analisados. Finalmente, com relação à técnica que avaliou morte celular neuronal, o grupo diabético apresentou três vezes mais marcações de neurônios fluorescentes, ou seja, com morte celular quando comparado com o grupo controle. Portanto, esses resultados sugerem que o EO pode representar um mecanismo envolvido nos efeitos da hiperglicemia no SNC de ratos neonatos. Além disso, as alterações na expressão de proteínas envolvidas em vias de sobrevivência/morte celular colaboram para o resultado de morte celular verificado no cérebro de animais com hiperglicemia neonatal e mostram os efeitos nocivos da DN em um período crucial de desenvolvimento cerebral. / Diabetes is an endocrine disorder of the carbohydrates metabolism clinically characterized by hyperglycemia, resulting from the inability of the body to secrete insulin, defeats in its action and both. In the last decade, there has been an increasing number of studies about neonatal diabetes (DN), a type of diabetes non-immunological diagnosed before 6 months of life. The most studies related to DN was developed in patients and mainly deal with clinical, etiological and therapeutic aspects. However, there is a few of studies in animal models in order to assess molecular damage in tissues submitted to neonatal hyperglycemia. Recently, the consequences of diabetes in the central nervous system (CNS) have received increased attention, as recent studies show that hyperglycemia is capable of promoting the rupture of redox homeostasis in the rat brain. Wherefore, the present work aimed to study not only the relationship between EO and neonatal hyperglycemia in rat brain, but also evaluate if the oxidative damage promoted by reactive oxygen species (ROS) in the hyperglycemic condition may be involved in the neuronal cell death process. For this, 5-day-old Wistar rats were used to promote the induction of diabetes, which was done with a single intraperitoneal streptozotocin (STZ) administration (100 mg/kg body weight). Rats with glycemia> 200 mg/dL were considered diabetic. The rats were sacrificed in 10 days of life, wherefore five days after STZ adiminstration. The whole brain of the rats was homogenized, centrifuged and homogenized used for EO techniques and protein expression measurements. In addition, total brain was used in histological sections for analysis of the neuronal cell death. The EO parameters evaluated were the activity of the glutathione S-transferase (GST), glutathione reductase (GR), glutamate-cystein ligase (GCL) and the determination of total and reduced glutathione concentration (GSH/GSSG). Hydrogen peroxide (H2O2) was evaluated along with Western Blot protein quantification of catalase (CAT), glutathione peroxidase (GPx), heme oxygenase (HO-1) and thioredoxin (TRX). Relative to cell survival and death were evaluated protein kinase B (Akt), phosphorylated protein kinase B (p-Akt), glycogen synthase kinase 3β (GSK3β), p38 mitogen-activated protein kinase (p38), c-Jun amino-terminal kinases (JNK), phosphorylated c-Jun amino-terminal kinases (p-JNK), B-cell 10 lymphoma 2 (Bcl2) and Bcl2-associated protein X (Bax) by western blot. The neonatal hyperglycemia was not able to promote significant differences in the glutathione metabolism (GST, GR, GCL and GSH / GSSG) nor in the H2O2 measurement when compared to the control group. Nrf2 protein expression was decreased whereas CAT, HO-1 and TRX protein expression were increased in the diabetic group when compared to the control group. No significant differences were found in the protein expression of SOD and GPx. Also, p38 and Bcl2 protein expression was increased, whereas p-Akt was decreased in the diabetic group, already regarding the expression of JNK, p-JNK, Jsk3β and Bax proteins there were no significant difference in the analyzed groups. Finally, relative to neuronal cell death technique, the diabetic group presented three fold more neuronal cell death with fluorescent marking characteristic, when compared to the control group. Therefore, these results suggest that OE may represent a mechanism involved in the effects of hyperglycemia in the central nervous system of neonatal rats. In addition, changes in the expression of proteins involved in survival/death cell pathways contribute to the outcome of cell death, result found in the brain of animals with neonatal hyperglycemia and finally show the harmful effects of neonatal diabetes in a crucial period of brain development.
237

Efeito do consumo de frutas, legumes e verduras na saúde cardiovascular em adolescentes: uma revisão sistemática / Effect of fruit and vegetable consumption on cardiovascular health in adolescents: a systematic review

Collese, Tatiana Sadalla 10 February 2017 (has links)
Introdução: O consumo de frutas, legumes e verduras é pouco frequente entre os adolescentes, e o possível efeito deste consumo na saúde cardiovascular durante esta faixa etária é indefinido. Objetivo: Verificar se existe associação entre o consumo de frutas, legumes e verduras e indicadores de risco cardiovascular em adolescentes (obesidade abdominal, hiperglicemia, hipertrigliceridemia, dislipidemia, hipertensão arterial sistêmica, e síndrome metabólica). Métodos: Registrou-se esta revisão sistemática no PROSPERO (CRD42013004818) para realizar uma revisão sistemática em seis bases de dados eletrônicas (Biomed Central, CINAHL, MEDLINE, PsycINFO, Scopus, Web of Science). Considerou-se o período desde a criação destas bases de dados até sete de Dezembro de 2015 como data mais recente para a atualização das buscas. A estratégia de busca utilizou os seguintes grupos de descritores: faixa etária; frutas, legumes e verduras; indicadores de risco cardiovascular; estudos transversais ou coorte. Os critérios de elegibilidade foram: Artigos em Inglês, Espanhol e Português? estudos originais? amostra composta de adolescentes (dez a 19 anos de idade segundo a organização mundial de saúde); descritores de acordo com os indicadores de risco cardiovascular estabelecidos para adolescentes. Artigos potencialmente elegíveis foram selecionados por dois revisores separadamente. Resultados: Foram identificados 5632 artigos. Após a leitura dos títulos e resumos, 102 artigos potencialmente relevantes permaneceram para a leitura na íntegra. Após seleção, 11 artigos preencheram os critérios de elegibilidade e foram incluídos (dez transversais, uma coorte). As principais razões para a exclusão dos estudos foram classificação da adolescência diferente da preconizada pela Organização Mundial de Saúde, o consumo de frutas, legumes e verduras analisado como parte de um padrão alimentar (por exemplo, juntamente com peixes, laticínios ou cereais), e os indicadores de risco cardiovascular que não foram especificados ou que diferiram das definições estabelecidas. Os artigos avaliaram a ingestão de frutas, legumes e verduras em diversas unidades de medida, utilizando-se questionários de frequência de consumo alimentar (54.5%), recordatório alimentar de 24 horas (27.3%) e registro alimentar (18.2%). Além disso, o consumo de frutas, legumes e verduras foi avaliado separadamente (54.5%), em conjunto (36.4%), apenas legumes e verduras (9.1%), e um estudo incluiu suco de frutas (9.1%). Um terço dos estudos mostraram associações significativas entre o consumo de frutas, legumes e verduras e a pressão arterial sistólica, obesidade abdominal, triglicérides, HDL colesterol e síndrome metabólica. Conclusão: As associações entre o consumo de frutas, legumes e verduras e indicadores de risco cardiovascular em adolescentes são inconsistentes. Isto se deve provavelmente à heterogeneidade nos métodos utilizados para avaliar/classificar o consumo e/ou definir o risco cardiovascular neste grupo etário. Uma vez que os benefícios deste consumo já são bem estabelecidos na saúde cardiovascular de adultos, ainda são necessários estudos adicionais que abordem alta qualidade metodológica para melhor compreender esse fenômeno nos adolescentes / Background: Fruit and vegetable consumption is infrequent among adolescents, and the possible effect of this consumption on cardiovascular health during this age group is undefined. Aim: To investigate the association between fruit and vegetable consumption on cardiovascular risk indicators in adolescents (abdominal obesity, hyperglycemia, hypertriglyceridemia, dyslipidemia, hypertension and metabolic syndrome). Methods: This systematic review was registered in PROSPERO (CRD42013004818), and a systematic review searching electronic databases (Biomed Central, CINAHL, MEDLINE, PsycINFO, Scopus, Web of Science) from inception to December 7, 2015 was conducted. The search strategy used the following sets of descriptors related to: age group; fruits and vegetables; cardiovascular risk indicators; cross-sectional and cohort studies. Eligibility criteria were: Articles in English, Spanish and Portuguese; original studies; sample of adolescents (10-19 year-old according to World Health Organization); descriptors according to the cardiovascular risk indicators. Potentially eligible articles were selected by two reviewers separately. Results: A total of 5632 articles were identified. After reading the titles and abstracts, 102 potentially relevant articles remained for full reviewed. After selection, 11 articles meeting the inclusion criteria were included (10 cross-sectional; 1 cohort). The main reasons for study exclusion were misclassifying adolescence, assessing fruits and vegetables as part of a food pattern (for example, together with fish, dairy, or cereal), and cardiovascular risk indicators that were not specified or that differed from the definitions established. Articles evaluated fruit and vegetable intake in diverse units, using food frequency questionnaires (54.5%), 24-hour-dietary-recalls (27.3%), and food records (18.2%). In addition, fruit and vegetable consumption were assessed separately (54.5%), together (36.4%), or only vegetables (9.1%); and 1 article included fruit juice (9.1%). A third of the studies showed significant inverse associations of fruit and vegetable intake with systolic blood pressure, abdominal obesity, triglycerides, HDL cholesterol, and metabolic syndrome. Conclusion: The associations between fruit and vegetable consumption and adolescent cardiovascular risk indicators are inconsistent. Since the benefits of this consumption are well established in adult cardiovascular health, further studies are necessary, addressing high methodological quality to better understand this phenomenon in adolescents
238

Hyperglycemia and Focal Brain Ischemia : Clinical and Experimental Studies

Farrokhnia, Nasim January 2005 (has links)
<p>Diabetes is a major risk factor for ischemic stroke and is associated with increased mortality. Additionally, hyperglycemia, a common complication in acute stroke, is associated with poor outcome.</p><p>In order to identify the correlation between blood glucose and early mortality, multiple logistic regression analyses were used and odds ratios calculated in a retrospective study of 447 stroke patients. Eighty-one patients (18%) had diabetes. The odds ratios for 30-day case-fatality and blood glucose were 1.9 and 1.6 in diabetic and non-diabetic patients respectively. Optimal blood glucose concentrations in respective group were 10.3 and 6.3 mmol/L, as determined by receiver operator characteristic (ROC) curves.</p><p>Cerebral ischemia triggers different signaling pathways including mitogen-activated protein kinases (MAPK) which regulate fundamental cell functions. In an experimental rat model of combined hyperglycemia and transient middle cerebral artery occlusion (MCAO), the activation pattern of one such MAPK, extracellular signal-regulated kinase (ERK) was studied along with infarct volumes and neurological function. Hyperglycemia resulted in markedly increased ERK activation and approximately three-fold increase of infarcts compared with controls. </p><p>Based on the increased ERK activation, further experiments were conducted to limit the hyperglycemic-ischemic damage by interfering with ERK and supposedly related mechanisms. Consequently, rats were given U0126 (inhibiting ERK activation), PBN (anti-oxidative), PP2 (inhibiting src-family kinases), or vehicle. PBN reduced infarcts and improved neurological function compared with controls while no statistically significant effects were observed for U0126 or PP2. However, when the dose was doubled, U0126 significantly reduced infarcts and improved neurological function after 1 day in hyperglycemic rats. Post-ischemic ERK activation was completely inhibited by U0126 as demonstrated with Western immunoblotting. The findings suggest that ERK is an important mediator of hyperglycemic-ischemic brain injury and possible target for future interventions.</p>
239

Hyperglycemia and Focal Brain Ischemia : Clinical and Experimental Studies

Farrokhnia, Nasim January 2005 (has links)
Diabetes is a major risk factor for ischemic stroke and is associated with increased mortality. Additionally, hyperglycemia, a common complication in acute stroke, is associated with poor outcome. In order to identify the correlation between blood glucose and early mortality, multiple logistic regression analyses were used and odds ratios calculated in a retrospective study of 447 stroke patients. Eighty-one patients (18%) had diabetes. The odds ratios for 30-day case-fatality and blood glucose were 1.9 and 1.6 in diabetic and non-diabetic patients respectively. Optimal blood glucose concentrations in respective group were 10.3 and 6.3 mmol/L, as determined by receiver operator characteristic (ROC) curves. Cerebral ischemia triggers different signaling pathways including mitogen-activated protein kinases (MAPK) which regulate fundamental cell functions. In an experimental rat model of combined hyperglycemia and transient middle cerebral artery occlusion (MCAO), the activation pattern of one such MAPK, extracellular signal-regulated kinase (ERK) was studied along with infarct volumes and neurological function. Hyperglycemia resulted in markedly increased ERK activation and approximately three-fold increase of infarcts compared with controls. Based on the increased ERK activation, further experiments were conducted to limit the hyperglycemic-ischemic damage by interfering with ERK and supposedly related mechanisms. Consequently, rats were given U0126 (inhibiting ERK activation), PBN (anti-oxidative), PP2 (inhibiting src-family kinases), or vehicle. PBN reduced infarcts and improved neurological function compared with controls while no statistically significant effects were observed for U0126 or PP2. However, when the dose was doubled, U0126 significantly reduced infarcts and improved neurological function after 1 day in hyperglycemic rats. Post-ischemic ERK activation was completely inhibited by U0126 as demonstrated with Western immunoblotting. The findings suggest that ERK is an important mediator of hyperglycemic-ischemic brain injury and possible target for future interventions.
240

Diabetes and Endoplasmic Reticulum Stress in Pancreatic beta-cells: Effects on Insulin Biosynthesis and beta-cell Apoptosis

Lai, Elida Wing Shan 30 July 2008 (has links)
Chronic hyperlipidemia (lipotoxicity) and hyperglycemia (glucotoxicity) have recently been shown to induce Endoplasmic Reticulum (ER) stress, which may contribute to pancreatic beta-cell dysfunction in type 2 diabetes. This thesis examined the involvement of ER stress in beta-cell lipotoxicity and glucotoxicity. Although chronic treatment with saturated free fatty acids (FFA) in vitro induced ER stress, altering ER stress by increasing or knocking-down GRP78 chaperone expression had no effect on apoptosis induction. Conversely, overexpression of ER chaperones rescued the reduction in proinsulin protein levels caused by chronic exposure to high glucose, although it had no effect on the decreased insulin mRNA levels and proinsulin translation rate. Thus, ER stress is likely not the main mechanism involved in saturated FFA-induced beta-cell apoptosis in vitro, but it may contribute to glucotoxic effects on proinsulin levels. These findings have increased our understanding of the link between ER stress and beta-cell dysfunction in type 2 diabetes.

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