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  • Open Access

17 October 2024

12 Pages

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

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1
Service of Endocrinology, University Hospital of the Federal University of Maranhão (HUUFMA/EBSERH), São Luís 65020-070, Brazil
2
Research Group in Endocrinology and Clinical and Molecular Metabolism (ENDOCLIM), Sao Luis 65020-070, Brazil
3
Post-Graduate Program in Adult Health (PPGSAD), Federal University of Maranhão (UFMA), São Luis 65085-580, Brazil
4
DNA Diagnostic Laboratory (LDD), Rio de Janeiro State University (UERJ), Rio de Janeiro 20550-900, Brazil
This article belongs to the Special Issue Neuroendocrinology Across Time

Abstract

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.

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