RESUMOObjetivo: 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 tolerân-cia 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% 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 insulíni-ca (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 índices de avaliação da secreção pancreática devem ser corrigidos para o grau de resistên-cia insulínica, de modo a refletir melhor a história natural do diabetes mellitus. ABSTRACT Insulin Resistance and Secretion Assessment across a Range of GlucoseTolerance from Normal Individuals through Diabetes. 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% female. We allocated them in four groups: group 0 (normal): individuals with BMI < 25 Kg/m 2 and normal glucose metabolism, group 1 (obese): BMI ≥ 25 Kg/m 2 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 < ...
Insulin signalling pathways were investigated in a 33 year-old woman with immunologic insulin resistance. Her past medical history was remarkable for intermittent use of insulin and allergic reactions to several drugs, and measure of plasma anti-insulin antibodies level corroborated the clinical suspicion of immune mediated insulin resistance (8074 nU/ml - RIA - Ref value: <60). Treatment with several immunosuppressive regimens was tried, however the results were disappointing. Possible subcellular mechanisms of insulin resistance were investigated by performing analysis of insulin receptor and post receptor signaling in skeletal muscle biopsy. The expression of insulin receptor (IR), insulin receptor substrate 1 (IRS-1) and glucose transporter 4 (GLUT-4) was evaluated in total extract from muscle tissue by Western blotting. Basal IR, IRS-1 and GLUT-4 expression was detected, however receptor autophosphorylation was not observed. A study of translocation of GLUT-4 to plasma membrane showed that tissue presented low levels of membrane-associated GLUT-4. When in vitro stimulation was undertaken, tissue was capable to be responsive to insulin. Our results suggest that even though IR expression was normally occurring, IR β-subunit tyrosine kinase activity in muscle was down-regulated leading to alterations in insulin post receptor signaling. Consistent with normal insulin receptor and post receptor signaling, our results were compatible with decreased insulin binding to IR probably due to neutralization by anti-insulin antibodies. In conclusion, this patient has immunologic insulin resistance and treatment should be based on immunosuppressive drugs as tolerated.
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