Ejercicio físico interválico de alta intensidad mejora el control glicémico y la capacidad aeróbica en pacientes con intolerancia a la glucosa / High intensity interval training improves glycemic control and aerobic capacity in glucose intolerant patients

Background: Proper exercise training modifies intra miocellular energy utilization, glucose transport and mitochondrial biogenesis. Aim: To determine the therapeutic effects of a high intensity intermittent training (HIIT) program on glucose homeostasis, physical fitness and body fat in glucose intolerant patients. Patients and Methods: Eighteen patients with overweight or obesity and glucose intolerance were invited to participate in an exercise program consisting in three sessions per week for 3 months. Ten participants aged 35 ± 13 years who attended > 26 of the planned 36 sessions, were considered as adherent to exercise. The other eight participants aged 37 ± 17 years, who attended to a mean of 13 sessions, were considered as non-adherent. Both groups had similar body weight, body mass index, body fat, plasma glucose 2 h after an oral glucose load and maximal oxygen uptake. All these variables were measured at the end of exercise intervention. Each session consisted of 1 min exercise of cycling at maximal intensity until muscle fatigue followed by 2 min rest, repeated 10 times. Results: Among adherent participants, twelve weeks of HIIT improved signifcantly maximal oxygen uptake (6.1 + 3.6 mL/kg/min or 24.6%), reduced 2 h post load blood glucose (-33.7 + 47.9 mg/dL or -12.5%) and body fat (-4.3 + 5.6 kg). No signifcant changes were observed in the non-adherent group. Conclusions: HIIT exercise reduces blood glucose after an oral load in glucose intolerant patients.

Obesity associated pathophysiological & histological changes in WNIN obese mutant rats.

Background & objectives: WNIN/Ob (obese and euglycaemic) and WNIN/GR-Ob (obesity with impaired glucose tolerance), were isolated and established from Wistar rat stock (WNIN). Both strains showed physical, physiological and biochemical indices related to obesity. We present here haematology, histology and pathophysiological changes between the phenotypes of these strains, lean (+/+), carrier (+/-) and obese (-/-). Methods: A total of 72 animals of equal gender consisting of three phenotypes were used for the study. Haematology, organ weights were measured and histopathology of the tissues studied using standard procedures. In 12 lean and obese rats (equal gender) of WNIN/GR-Ob group morphometry of pancreatic islets was done immunohistochemically (IHC). Results: Obese rats of both the strains showed normal haematology (except low platelet count), but exhibited changes in the organ weights and in histopathology in organs like liver, kidney, brain and testis/ovary. Hyperplasia of adipocytes was seen in obese rats as compared to lean and carrier. IHC of obese rat pancreas showed that both islet density and volume were significantly (P<0.05) increased compared to lean littermates. Interpretation & conclusions: The histological and pathophysiological changes seen in these mutants were in tune with obese phenotype exhibited by these animals.

Pathophysiology of type 2 diabetes mellitus in youth: the evolving chameleon / Fisiopatologia do diabetes melitotipo 2 no jovem: um camaleão em evolução

Type 2 diabetes mellitus (T2DM) in children and adolescents is an important Public Health problem against the backdrop of the epidemic of childhood obesity. The clinical presentation of T2DM in youth is heterogeneous from minimal symptomatology to diabetic ketoacidosis. The increasing rates of youth T2DM have paralleled the escalating rates of obesity, which is the major risk factor impacting insulin sensitivity. Additional risk factors include minority race, family history of diabetes mellitus, maternal diabetes during pregnancy, pubertal age group and conditions associated with insulin resistance (IR) - such as polycystic ovary syndrome (PCOS). The pathophysiology of T2DM has been studied extensively in adults, and it is widely accepted that IR together with beta-cell failure are necessary for the development of clinical diabetes mellitus in adulthood. However, pathophysiologic studies in youth are limited and in some cases conflicting. Similar to adults, IR is a prerequisite, but beta-cell failure is necessary for progression from normal glucose tolerance to prediabetes and frank diabetes in youth. Even though rates of T2DM in youth are increasing, the overall prevalence remains low if compared with type 1 diabetes mellitus (T1DM). However, as youth with T1DM are becoming obese, the clinical distinction between T2DM and obese T1DM has become difficult, because of the overlapping clinical picture with evidence of islet cell autoimmunity in a significant proportion of clinically diagnosed youth with T2DM. The latter are most likely obese children with autoimmune T1DM who carry a misdiagnosis of T2DM. Further research is needed to probe the pathophysiological, immunological, and metabolic differences between these two groups in the hopes of assigning appropriate therapeutic regimens. These challenges combined with the evolving picture of youth T2DM and its future complications provide unending opportunities for acquisition of new knowledge ...

Em um cenário de uma epidemia de obesidade, o diabetes melito tipo 2 (DM2) em crianças e adolescentes é um importante problema de Saúde Pública. As manifestações clínicas do DM2 na juventude são heterogêneas e vão desde sintomas leves até a cetoacidose diabética. As taxas crescentes de DM2 no jovem seguem em paralelo ao aumento da obesidade, a qual constitui o mais importante fator de risco para a redução da sensibilidade à insulina. Outras condições de risco para o DM2 são: minorias étnicas, história familiar de DM2, diabetes materno durante a gestação, idade puberal e situações associadas à resistência à insulina (RI) - como a síndrome dos ovários policísticos (SOP). A fisiopatologia do DM2 tem sido muito estudada em adultos, sendo aceita como condições necessárias à RI em conjunto com a disfunção da célula beta. Estudos da fisiopatologia em jovens são escassos e conflitantes. Semelhante ao que se passa com os adultos, a RI é um pré-requisito, mas a falência da célula beta é necessária para que haja progressão da tolerância normal à glicose para o pré-diabetes e DM2. Mesmo com o aumento da incidência de DM2 no jovem, a prevalência permanece baixa em comparação com o diabetes mellitus tipo 1 (DM1). Se uma criança com DM1 é obesa, a distinção clínica entre o DM2 e DM1 é dificultada, pois existem semelhanças clínicas e evidências da presença de autoimunidade contra a célula beta em uma significativa proporção de jovens diagnosticados com DM2. Esta condição normalmente representa uma criança obesa com autoimunidade para DM1 com o diagnóstico equivocado de DM2. Novas pesquisas são necessárias para caracterizar os diferentes mecanismos fisiopatológicos, imunológicos e metabólicos entre estes dois grupos, na esperança de que sejam alcançados regimes terapêuticos apropriados. Esses desafios e o quadro em mutação do diabetes na criança e no adolescente nos fornecem oportunidades infindáveis para a aquisição de novos conhecimentos no campo da diabetologia.

Avaliação da secreção e resistência insulínica em indivíduos com diferentes graus de tolerância à glicose - do metabolismo normal ao diabetes mellitus / Insulin resistance and secretion assessment across a range of glucose tolerance from normal individuals through diabetes

OBJETIVO: Os principais objetivos são determinar a associação entre os parâmetros clínicos e demográficos e os diferentes índices de secreção e resistência insulínica em indivíduos aparentemente saudáveis, sem conhecimento prévio de seu grau de tolerância à glicose. PACIENTES E MÉTODOS: Submetemos ao teste oral de tolerância à glicose (TOTG), no período de fevereiro a agosto de 2003, 105 indivíduos com média de idade de 33,4 ± 1,4 anos, sendo 57,1 por cento do sexo feminino, subdividindo-os em 4 grupos: grupo 0 (normais): indivíduos com IMC < 25 e metabolismo glicídico normal, grupo 1 (obesos): IMC > 25 e metabolismo glicídico normal, grupo 2 (IFG): glicemia de jejum alterada e grupo 3 (IOG): intolerância oral à glicose. RESULTADOS: Encontramos diferença estatística para todas as variáveis analisadas durante o TOTG dentre os 4 grupos de indivíduos: glicemias de jejum e em 2 horas (p < 0,05; p < 0,05), valor de pico (p < 0,05), delta (p = 0,02), percentual de incremento (p = 0,047), área sob a curva (p < 0,05) e tempo de pico da glicose (p = 0,022). Não encontramos diferença para a velocidade de incremento da glicose, assim como para nenhuma variável da curva de insulina. Em relação aos índices de secreção insulínica, não houve significância estatística para os índices insulinogênico ou delta, porém estes tornaram-se significantes após correção da secreção pela resistência insulínica (p = 0,008). Quanto aos índices de resistência insulínica, os índices HOMA e QUICKI foram estatisticamente significativos (p = 0,005; p = 0,005, respectivamente), assim como a relação glicose/insulina em jejum (p = 0,053). CONCLUSÃO: Apesar do tamanho limitado da amostra, podemos inferir que indivíduos com intolerância à glicose em jejum e pós-prandial possivelmente estão em momentos diferentes da história natural da doença. Nossos dados demonstram que os melhores índices para a avaliação de resistência insulínica são o HOMA e o QUICKI, e que os...

AIM AND METHODS: Our main aim was to determine the association between clinical, demographical parameters and different insulin resistance and secretion indices in apparently healthy subjects, without previous knowledge of their own level of glucose tolerance. For that purpose, we evaluated 105 individuals from February to August 2003 by means of OGTT, aged 33.4 ± 1.4 years old, 57.1 percent female. We allocated them in four groups: group 0 (normal): individuals with BMI < 25 Kg/m² and normal glucose metabolism, group 1 (obese): BMI > 25 Kg/m² and normal glucose metabolism, group 2 (IFG): impaired fasting glucose and group 3 (IGT): impaired glucose tolerance. RESULTS: We have found statistical difference on all variables during OGTT between all groups: fasting glucose (p < 0.05), 2-hour glucose (p < 0.05), glucose peak value (p < 0.05), glucose delta (p = 0.02), glucose incremental percentage (p = 0.047), area under curve (p < 0.05), and glucose peak time (p = 0.022). We have not found difference on any variable in insulin curves or on glucose incremental velocity. Regarding insulin secretion indices there were no statistical significance in insulinogenic or delta indices, but they became significant after being corrected by insulin resistance (p = 0.008). When we evaluated insulin resistance alone, by using HOMA and QUICKI indices and the fasting glucose to insulin index, we have found statistical significance (p = 0.005; p = 0.005; p = 0.053). CONCLUSION: Although studying a small sample, we could suggest that individuals with impaired fasting glucose and impaired glucose tolerance are in different stages of diabetes natural history disease. We found out that the best indices of insulin resistance are both HOMA and QUICKI. We also suggest that pancreatic secretion indices should be corrected by the insulin resistance, which could best reflect type 2 diabetes natural history.

Modificaciones dinámicas en los islotes de Langerhans de dos Líneas de ratas espontaneamente diabeticas / Dynamic modifications in islets of Langerhans in two lines of spontaneously diabetic rats

La rata eSMT derivó del cruzamiento de eSS y b, líneas de la cepa IIM. eSS es un modelo de diabetes tipo 2 sin sobrepeso; b desarrolla obesidad moderada e intolerancia tardía a la glucosa. Fueron comparados características metabólicas y hallazgos histopatológicos del páncreas endocrino entre eSS y eSMT. Cotejados con eSS, los animales eSMT jóvenes son más corpulentos y desarrollan hiperglucemia de ayuno e intolerancia a la glucosa más precoces e intensas. En los machos eSMT de 6 y 9 meses existen islotes de formas alteradas y con fibrosis, detectándose esporádicas imágenes de apoptosis. En los de un año se tornan más pequeños y escasos, remedando la histoarquitectura de los machos eSS en el segundo año de vida; posteriormente los islotes van disgregándose, a la vez que muestran ocasionales mitosis y se observa nesidioblastosis. Se sugiere que estas modificaciones dinámicas constituyen una respuesta a la hiperglucemia. Las hembras eSS conservan por más tiempo la estructura insular y tienen menores alteraciones de la glucemia. El dimorfismo sexual del síndrome diabético de eSMT es atenuado respecto de eSS. La construcción de una tipología de individuos mediante el análisis multivariado separó tres clusters, evidenciando diferencias genéticas, etáreas y de sexo.

The eSMT rat is derived from the crossing of eSS and b, both lines belonging to the IIM strain, while eSS is a model of type 2 diabetes without overweight and b develops moderate obesity and late glucose intolerance. Metabolic characteristics and histopathological findings in endocrine pancreas of eSS and eSMT were compared. Young eSMT animals are more robust than eSS and develop more intense fasting hyperglycemia and glucose intolerance at an earlier age. eSMT males of 6 and 9 months show islets with altered shapes and fibrosis, as well as sporadic images of apoptosis. At 12 months of age, islets are reduced in number and size, resembling the histoarchitecture of eSS males during their second year of life; eventually islets undergo disruption and, at the same time, occasional mitoses and nesidioblastosis are seen. These dynamic modifications may be expressing a response to hyperglycemia. eSS females preserve their insular structure for a longer time and have less glycemic alterations. Sexual dimorphism of the diabetic syndrome of eSMT is attenuated when compared with eSS. The construction of a typology of individuals through multivariate analysis separated three clusters, evidencing genetic, age and sex differences.

Diabetes melito: uma importante co-morbidade da fibrose cística / Diabetes mellitus in patients with cystic fibrosis

Diabetes melito relacionado à fibrose cística (DMFC) é a principal complicação extrapulmonar da fibrose cística. Atualmente, ele afeta 15-30 por cento dos adultos com fibrose cística e sua prevalência tende a aumentar com o aumento da expectativa de vida desses pacientes. Esse trabalho tem por objetivo rever a fisiopatologia, morbidade, manifestações clínicas, diagnóstico e tratamento do DMFC. Uma pesquisa bibliográfica utilizou os bancos de dados Medline e Literatura Latino-Americana e do Caribe em Ciências da Saúde, selecionando artigos publicados nos últimos vinte anos. A insulinopenia secundária à destruição de células beta pancreáticas é o principal mecanismo causal, embora a resistência insulínica também possa estar presente. O DMFC apresenta características do diabetes melito tipo 1 e tipo 2 e tem início, em média, aos 20 anos de idade. Ele pode cursar com hiperglicemia em jejum, pós-prandial ou intermitente. As alterações do metabolismo glicêmico agravam o estado nutricional, aumentam a morbidade, diminuem a sobrevida e pioram a função pulmonar. As complicações microvasculares estão presentes, porém raramente observam-se as macrovasculares. A triagem para o DMFC deve ser anual, a partir dos 10 anos de idade, através do teste de tolerância oral à glicose e, em qualquer faixa etária, se houver perda ponderal inexplicada ou sintomatologia de diabetes. Pacientes hospitalizados também devem ser investigados e receber terapia insulínica se a hiperglicemia em jejum persistir além de 48 h. A insulina é o tratamento de escolha para o diabetes com hiperglicemia em jejum. Não existe consenso quanto ao tratamento do diabetes intermitente ou sem hiperglicemia de jejum. Não há orientações de restrições alimentares. O acompanhamento deve ser multidisciplinar.

Cystic fibrosis-related diabetes (CFRD) is the principal extra-pulmonary complication of cystic fibrosis, occurring in 15-30 percent of adult cystic fibrosis patients. The number of cystic fibrosis patients who develop diabetes is increasing in parallel with increases in life expectancy. The aim of this study was to review the physiopathology, clinical presentation, diagnosis and treatment of CFRD. A bibliographic search of the Medline and Latin American and Caribbean Health Sciences Literature databases was made. Articles were selected from among those published in the last twenty years. Insulin deficiency, caused by reduced beta-cell mass, is the main etiologic mechanism, although insulin resistance also plays a role. Presenting features of type 1 and type 2 diabetes, CFRD typically affects individuals of approximately 20 years of age. It can also be accompanied by fasting, non-fasting or intermittent hyperglycemia. Glucose intolerance is associated with worsening of nutritional status, increased morbidity, decreased survival and reduced pulmonary function. Microvascular complications are always present, although macrovascular complications are rarely seen. An oral glucose tolerance test is recommended annually for patients e" 10 years of age and for any patients presenting unexplained weight loss or symptoms of diabetes. Patients hospitalized with severe diseases should also be screened. If fasting hyperglycemia persists for more than 48 h, insulin therapy is recommended. Insulin administration remains the treatment of choice for diabetes and fasting hyperglycemia. Calories should not be restricted, and patients with CFRD should be managed by a multidisciplinary team.

Disfunção autonômica cardiovascular no diabetes mellitus experimental / Cardiovascular autonomic dysfunction in experimental diabetes mellitus

Muitas informações novas têm sido publicadas nos últimos anos a respeito da fisiopatologia da disfunção autonômica cardiovascular em ratos e camundongos diabéticos. Nosso grupo tem estudado o curso temporal das alterações cardiovasculares associadas ao diabetes experimental há alguns anos, obtendo evidências consistentes de grave disautonomia em modelos animais de diabetes. O objetivo deste trabalho foi revisar a contribuição que estudos envolvendo diferentes modelos de deficiência e resistência à insulina têm fornecido para o entendimento, tratamento e prevenção da disfunção autonômica cardiovascular do diabetes.

Much new information has been published in the last few years regarding pathophysiology of cardiovascular autonomic dysfunction in diabetic rats and mice. Our group has been studying the time-course cardiovascular changes associated with experimental diabetes in the last years, and obtained consistent evidences of severe dysautonomia in diabetes animal models. The aim of this manuscript is to review the contribution that studies involving different animal models of insulin deficiency or resistance have given to understand, treat and prevent diabetic cardiovascular autonomic dysfunction.

O papel da lipemia pós-prandial na gênese da aterosclerose: particularidades do diabetes mellitus / The role of post-prandial lipids in atherogenesis: particularities of diabetes mellitus

A aterosclerose é uma doença multifatorial e complexa, que determina eventos clínicos causadores de morbi-mortalidade significativa, representada pela ocorrência de infarto agudo do miocárdio, angina e morte súbita. Está associada a anormalidades lipídicas, ativação plaquetária, trombose, inflamação, disfunção endotelial, estresse oxidativo e alterações metabólicas da matriz, entre outros distúrbios. Todas essas anormalidades são mais comuns e acentuadas no paciente com diabetes, assim como no estado pós-prandial. Dentre os fatores de risco para doença arterial coronariana que ainda não são efetivamente empregados nas estratégias de prevenção da doença em grandes populações destaca-se a hiperlipemia pós-prandial, possível marcador precoce de anormalidades metabólicas e disfunção vascular não observadas em jejum. Recentes resultados mostram que as alterações que ocorrem após uma única sobrecarga lipídica se relacionam negativamente à função endotelial, sendo que as alterações na reatividade vascular estão fortemente associadas à progressão da aterosclerose e aos eventos cardiovasculares. Essas alterações podem revelar um estado de intolerância às gorduras que já são detectadas em indivíduos saudáveis, antes mesmo que anormalidades em jejum sejam percebidas. Esta revisão aborda a fisiopatologia envolvida na lipemia pós-prandial e sua relação com a aterogênese, com ênfase no diabetes mellitus.

Atherosclerosis is a complex and multifactorial disease, which determines clinical events that cause significant morbi-mortality, represented by acute myocardial infarction, angina and sudden death. It is associated with lipid disturbances, platelet activation, thrombosis, endothelial dysfunction, inflammation, oxidative stress, altered matrix metabolism, among other disturbances. All these abnormalities are usual and more pronounced in diabetic patients, as well as in the post-prandial state. Among the coronary artery disease risk factors that are not usually employed in clinical practice in the whole population, postprandial hyperlipemia plays a major role, being a possible early marker of metabolic abnormalities and vascular dysfunction not yet seen in the fasting state. Recent results showed that post-oral lipid overload changes are negatively associated with endothelial dysfunction, and vascular reactivity abnormalities are strongly related to atherosclerosis progression and cardiovascular events. These abnormalities could disclose a lipid intolerance state that can be detected in apparently healthy subjects even before fasting abnormalities are seen. This review will deal with the pathophysiology changes involved in post-prandial hyperlipemia and its relationship with atherogenesis, with particular emphasis to diabetes mellitus.

Pathophysiology of prediabetes.

Type 2 diabetic patients pass through a phase of impaired glucose tolerence and/or impaired fasting glucose known as 'prediabetic state'. Prediabetic state form a part of syndrome X, other components being obesity, hypertension, dyslipidaemia, hyperinsulinaemia and insulin resistance. The pathophysiology of prediabetes is similar to type 2 diabetes mellitus, two basic defects are insulin resistance and early beta cell failure. In prediabetes, the rapid oscillations of insulin secretion are lost and amplitude of large pulses are decreased. When insulin is delivered in a pulsatile fashion that mimics the normal rapid oscillation, its hypoglycaemic effects are greater. In prediabetes, the glycaemic excursions after each meal are high and early insulin responses to meals tend to be lower than normal but the second phase of insulin secretion is delayed and prolonged.

Nutrition in prediabetes.

Impaired glucose tolerance (IGT) and impaired fasting glucose (IFG) are forerunners of type 2 diabetes mellitus (DM) and are now recognised as prediabetes states. Cardiovascular disease (CVD) is associated with these conditions and there are many studies such as the Da Quin IGT and DM study; Finnish Diabetes Prevention Study(DPS); The Diabetes Prevention Program(DPP) which have clearly shown the efficacy and supremacy of diet intervention in controlling progression of the prediabetes state to type 2 DM. Weight reduction, increasing physical activity and restricting not only total calories but also deriving them from more healthy sources by reducing the total intake of fat, changing n-6 PUFA to n-3 PUFA, increasing the intake of fibre rich carbohydrates and the use of antioxidants have not only long-term health benefits but also can be a very useful cost-effective tool to overcome the burden of type 2 DM in our country. Prevention of type 2 DM is not a dream but a reality and this can be achieved from a path through our kitchen. Faulty nutrition seems to be the main culprit in this wide-spread epidemic of diabetes and nutritional therapy in prediabetes state appears to be the only option in our hands.

Nerve conduction abnormalities in different stages of glucose intolerance.

AIMS: To look for changes in nerve conduction velocity (NCV) in early stages of glucose intolerance, i.e. in impaired glucose tolerance (IGT) and in asymptomatic newly diagnosed Type 2 diabetic subjects (NDD). MATERIALS AND METHODS: A total of 225 subjects were categorized as: Group 1: Subjects with normal glucose tolerance (NGT), Group 2: IGT subjects and Group 3: NDD subjects. Motor (MCV) and Sensory nerve Conduction Velocity (SCV) measurements were done. RESULTS: The mean MCV was significantly lower in the NDD group (47 +/- 5 m/s) when compared with the other two groups (IGT=50 +/-4.5 m/s; NGT= 53 +/- 4 m/s; P=0.0001). The IGT group of subjects also exhibited a significantly lower mean MCV when compared with the NGT subjects (P=0.0001). The mean SCV in the NDD group (42+10 m/s) was also significantly lower (P< 0.0007) than the NGT (46+6 m/s) and the IGT (48+10 m/s) groups. No significant difference in the mean SCV between the NGT and IGT groups was noted. In the multiple linear regression analysis both age and male gender were the risk factors for abnormal MCV and SCV. Abnormal MCV was found to be associated with 2-hr post glucose levels (R2 = 14.5%), while HbA1c (R2 = 4.9%) contributed towards abnormal SCV. CONCLUSION: Abnormal NCV is a common finding in NDD subjects. Slower mean MCV demonstrated by IGT subjects, calls for early screening of these subjects for complications.

Incidencia de intolerancia a los carbohidratos en pacientes de la consulta externa: estudio clínico prospectivo / Carbohydrate intolerance: its frequency in patients who attend to the out-patient care unit. Prospective trial

En este estudio se evaluaron a 117 pacientes sin diagnóstico previo de alguna enfermedad que alterara el metabolismo de los carbohidratos, a los que se aplicó una encuesta conteniendo diversos factores de riesgo y se realizaron las siguientes mediciones: talla, peso, circunferencia de cintura y cadera, presión arterial. Se les clasificó en tres grupos según el número de puntos de la encuesta: bajo 0-5, mediano 6-10 y alto riesgo más de 11 puntos. Por último, se les practicó una curva de tolerancia oral a la glucosa (CTOG). El 17.9 por ciento (20) correspondió al sexo masculino mientras que el 82.9 por ciento (97) correspondió al sexo femenino. El antecedente de riesgo más importante para diabetes mellitus fue tener un familiar de 1º y 2º grado, tener más de 40 años, no realizar ejercicio regularmente, tener un índice de masa corporal > 27, multiparidad e índice cintura cadera > 0.84. La incidencia de intolerancia a los carbohidratos fue de 23.9 por ciento, con diabetes mellitus 8.5 por ciento y 67.5 por ciento de individuos normales. Se observó que a los individuos ubicados en los grupos de mediano y alto riesgo según la encuesta es necesario considerar la realización de la CTOG. La glucosa plasmática en ayunas no fue el examen de escrutinio ideal. Se recomienda la aplicación de la encuesta como método de detección temprana, así como la CTOG como método de escrutinio después de la encuesta

Neuropatia vegetativa em pacientes com tolerância diminuida à glicose / Autonomic neuropathy in patients with impaaired glucose tolerance test

Com o objetivo de determinar se tolerância diminuída à glicose (TDG) está associada a neuropatia vegetativa realizamos estudo transversal de que participaram 44 pacientes com intolerância a glicose (Grupo 1)os quais foram comparados com 43 indivíduos controles apresentando teste de tolerância à glicose normal (Grupo 2). Os pacientes de ambos os grupos, após aceitarem participar da pesquisa, eram submetidos a anamnese, exames clínicos e laboratoriais e estudo da funçäo vegetativa (intervalo QT, prova da arritmia sinusal, manobra de Valsalva e teste postural). Os pacientes com TDG apresentaram mais hipertensao arterial sistêmica, obesidade contrípeta, hiperglicemias de jejum e pós-prandiais e dislipidemias que os controles. O teste de arritmia sinusal estava alterado em 54,5 por cento dos grupo 1 e em 32,5 por cento do grupo 2. A manobra de Valsalva foi anormal em 34,1 por cento no grupo 1 e em 7 por cento dos controles (p=0,004). A prova postural näo foi diferente nos dois grupos. O comprometimento do sistema neurovegetativo foi mais frequente nos pacientes com TDG que nos controles. A maior frequência de fatores de risco para doença aterosclerótica cardiovascular e o concomitante comprometimento do sistema nervoso vegetativo nos pacientes com TDG podem ser os responsáveis pelas elevadas taxas de letalidade devida a vasculopatias observadas nessa populaçäo.