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Relationship Between C-Peptide Levels, Clinical Features, and Serum Data in a Brazilian Type 1 Diabetes Population with Large Variations in Genomic Ancestry

2024; Multidisciplinary Digital Publishing Institute; Volume: 25; Issue: 20 Linguagem: Inglês

10.3390/ijms252011144

1661-6596

Rossana Santiago de Sousa Azulay, Vandílson Pinheiro Rodrigues, Débora Cristina Ferreira Lago, Ana Gregória Ferreira Pereira de Almeida, Joana D’Arc Matos França de Abreu, L. Matos, Caio Leônidas Oliveira de Andrade, Gilvan Cortês Nascimento, Marcelo Magalhães, Alexandre Facundo, Clariano Pires de Oliveira Neto, Adriana Guimarães Sá, Silva Da, Marília Brito Gomes, Manuel dos Santos Faria,

Diabetes Management and Research

Type 1 diabetes (T1D) is a chronic disease characterized by the immune-mediated destruction of the pancreatic beta cells responsible for insulin production. The secreted insulin and C-peptide are equimolar. Due to its longer half-life, C-peptide has become a safer means of assessing the pancreatic reserve. C-peptide levels were evaluated in a population of patients with T1D, focusing on the relationship between this variable and other factors. In addition, the influence of C-peptide on metabolic control and microvascular complications was investigated. This cross-sectional study included 95 patients who had been diagnosed with T1D at least five years earlier. These patients were evaluated using a clinical demographic survey, anthropometric data, laboratory tests, and fundoscopy. This study showed that 29.5% of patients had residual insulin secretion, which correlated directly with their age at diagnosis. No statistically significant differences in metabolic control or microvascular complications were observed between the C-peptide level groups. In addition, our results indicate that ancestry does not influence the persistence of residual C-peptide function in our highly mixed population. It is recommended that future research consider incorporating new variables, such as HLA and pancreatic autoimmunity, as factors that may influence residual β-cell function.