ArticleArchives of endocrinology and metabolism2024
Decoding the relationship between cow's milk proteins and development of type 1 diabetes mellitus.
Article in Archives of endocrinology and metabolism, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Immune Reactivity to Raw and Processed Foods and Their Possible Contributions to Autoimmunity.Foods (Basel, Switzerland) · 2025Review
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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