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DOI 10.20945/2359-4292-2023-0248

Медицинская библиотека · Archives of endocrinology and metabolism · 2024

Decoding the relationship between cow's milk proteins and development of type 1 diabetes mellitus.

Andrade Luís Jesuino de Oliveira, de Oliveira Gabriela Correia Matos, de Oliveira Luísa Correia Matos, Bittencourt Alcina Maria Vinhaes, Baumgarth Yvana, de Oliveira Luís Matos

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Аннотация

OBJECTIVE

To analyze in silico the evidence of molecular mimicry between human beta-cell autoantigens and cow's milk proteins as a potential type 1 diabetes mellitus (T1DM) trigger.

MATERIALS AND

METHODS

The in silico analysis was performed using bioinformatics tools to compare the amino acid sequences of cow's milk proteins (bovine serum albumin [BSA] and beta-lactoglobulin [BLG]) and human beta-cell autoantigens (glutamic acid decarboxylase-65 [GAD-65], insulin, and zinc transporter 8 [ZnT8]). The structural and functional characteristics of the proteins were analyzed to identify potential molecular mimicry mechanisms.

RESULTS

The results of the in silico analysis showed significant sequence similarity between BSA/BLG and GAD-65/human insulin/ZnT8, ranging from 19.64% to 27.27%. The cow's milk proteins evaluated shared structural features with the beta-cell antigens selected for comparison, indicating a potential for molecular mimicry between these proteins.

CONCLUSION

The findings of this study provide further evidence for a potential role of cow's milk proteins in triggering T1DM. The in silico analysis suggests that molecular mimicry mechanisms between cow's milk proteins and human beta-cell antigens may contribute to the autoimmune response leading to T1DM.

Для цитирования: Andrade Luís Jesuino de Oliveira, de Oliveira Gabriela Correia Matos, de Oliveira Luísa Correia Matos, Bittencourt Alcina Maria Vinhaes, Baumgarth Yvana, de Oliveira Luís Matos. Decoding the relationship between cow's milk proteins and development of type 1 diabetes mellitus.. Archives of endocrinology and metabolism. 2024. DOI: 10.20945/2359-4292-2023-0248.

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