ABSTRACT
OBJECTIVE: To investigate the growth hormone (GH) response to glucagon stimulation test (GST) in a population of healthy men over 50 years old in comparison to insulin tolerance test (ITT), analysis of the spontaneous 24-hour GH profile and insulin-like growth factor 1 (IGF-I). METHODS: 27 healthy men aged between 51 and 65 years were tested. RESULTS: Using non-parametric correlation analysis, a positive correlation between GH peak after GST and mean IGF-I (r = 0.528; p = 0.005) was found, as well with GH peak in 24-hour profile (r = 0.494; p = 0.009). No correlation was found comparing GH peak after ITT with the same parameters. Ten subjects presented GH peak of less than 3.0 μg/L after GST, none confirmed in ITT. CONCLUSIONS: GH peak response to GST was lower than ITT, but it showed a positive correlation with mean IGF-I and also with GH peak in 24-hour profile. However, GST should not be used to differentiate organic growth hormone deficiency (GDH) from the expected decline on GH secretion due to aging.
OBJETIVO: Investigar a resposta do hormônio do crescimento (GH) ao teste de estímulo com glucagon (GST) numa população de homens saudáveis acima dos 50 anos de idade, em comparação ao teste de tolerância à insulina (ITT), além da análise do perfil de secreção espontânea de GH nas 24 horas e fator de crescimento semelhante à insulina (IGF-I) basal. MÉTODOS: 27 homens, com idades entre 51 e 65 anos, foram submetidos aos testes. RESULTADOS: Utilizando análise de correlação não paramétrica, encontrou-se correlação positiva entre o pico de GH pós-GST e a média de IGF-I (r = 0,528; p = 0,005), e também com o pico espontâneo do GH no perfil de 24 horas (r = 0,494; p = 0,009). Não houve correlação do pico de GH pós-ITT com os mesmos parâmetros. Dez indivíduos apresentaram pico de GH após GST inferior a 3,0 μg/L, sem confirmação no ITT. CONCLUSÕES: O pico de GH pós-GST foi menor do que o obtido pós-ITT, porém demonstrou correlação positiva com a média de IGF-I e o pico de GH na secreção espontânea de 24 horas. Entretanto, o GST não demonstrou ser um bom teste para distinguir entre deficiência de hormônio de crescimento (DGH) e somatopausa.
Subject(s)
Aged , Humans , Male , Middle Aged , Glucagon , Human Growth Hormone , Insulin , Insulin-Like Growth Factor I/metabolism , Statistics, NonparametricABSTRACT
Stem cell factor (SCF) is a major mast cell growth factor, which could be involved in the local increase of mast cell number in the asthmatic airways. In vivo, SCF expression increases in asthmatic patients and this is reversed after treatment with glucocorticoids. In vitro in human lung fibroblasts in culture, IL-1beta, a pro-inflammatory cytokine, confirms this increased SCF mRNA and protein expression implying the MAP kinases p38 and ERK1/2 very early post-treatment, and glucocorticoids confirm this decrease. Surprisingly, glucocorticoids potentiate the IL-1beta-enhanced SCF expression at short term treatment, implying increased SCF mRNA stability and SCF gene transcription rate. This potentiation involves p38 and ERK1/2. Transfection experiments with the SCF promoter including intron1 also confirm this increase and decrease of SCF expression by IL-1beta and glucocorticoids, and the potentiation by glucocorticoids of the IL-1beta-induced SCF expression. Deletion of the GRE or kappaB sites abolishes this potentiation, and the effect of IL-1beta or glucocorticoids alone. DNA binding of GR and NF-kappaB are also demonstrated for these effects. In conclusion, this review concerns new mechanisms of regulation of SCF expression in inflammation that could lead to potential therapeutic strategy allowing to control mast cell number in the asthmatic airways.