Sensibilidade insulínica e função da célula beta após refeição mista em indivíduos com deficiência isolada do hormônio de crescimento

• Autor(a) principal: Santos, Paula Fernandes da Cunha
• Data de Publicação: 2019
• Tipo de documento: Trabalho de conclusão de curso
• Idioma: por
• Título da fonte: Repositório Institucional da UFS
• Texto Completo: https://ri.ufs.br/jspui/handle/riufs/15621
• topic: Hormônio de crescimento; Insulina; Célula beta; Growth hormone; Insulin; Beta Cell; CIENCIAS DA SAUDE::MEDICINA

Context: In Itabaianinha-SE, a population of 105 individuals with isolated growth hormone deficiency (DIGH) was described according to a mutation at the beginning of intron 1 of the growth hormone releasing hormone receptor (GHRHR) gene. These individuals were extensively studied from the metabolic point of view and, although they presented visceral obesity, increased blood pressure, total cholesterol and LDL and C-reactive protein, they exhibited better insulin sensitivity (SI) and reduced pancreatic beta cell function controls. This study was performed about 10 years ago using TTGO with 75g (the same used for diagnosis of diabetes mellitus). Objective: To reassess the insulin sensitivity and beta cell function in individuals with DIGH, after almost 10 years of follow-up; this time using a standardized test meal instead of oral glucose. Materials and methods: In a cross-sectional study of 20 subjects with DIGH and 20 controls, we measured blood glucose and insulin levels before and 30, 60, 120 and 180 min after a standardized test meal. HOMA-IR, HOMA-ß and areas under the curves (AUC) of glycemia and insulin were calculated. Results: HOMA-IR and fasting HOMA-ß were lower and the AUC for glycemia was higher in the DIGH than in controls (p = 0.002, p = 0.023, p = 0.0157, respectively). There was no difference in AUC for insulin. Conclusions: Ratifying data previously obtained with a different stimulus other than oral glucose, patients with congenital untreated IGHD throughout life expressed better insulin sensitivity and lower beta cell function than controls. This information suggests that enteroendocrine changes resulting from the GHRH receptor gene mutation may contribute to the normal life expectancy of these individuals, despite several cardiovascular risk factors.