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Latent autoimmune diabetes in adults (LADA) may initially resemble type 2 diabetes despite an autoimmune process that progressively compromises insulin secretion. This distinction becomes clinically important when glucagon-like peptide-1 receptor agonists (GLP-1RAs) or the dual glucose-dependent insulinotropic polypeptide/GLP-1 receptor agonist tirzepatide are considered. GLP-1RAs and tirzepatide are not approved for the glycemic treatment of LADA or type 1 diabetes. This narrative review examines the diagnosis and natural history of LADA, the evidence for incretin-based treatment, and the circumstances associated with diabetic ketoacidosis, including euglycemic presentations. The literature update focused on publications from 2020 to 2025, while retaining foundational studies relevant to disease classification and treatment safety. Autoantibody testing identifies an autoimmune etiology, whereas stimulated C-peptide measurement helps establish the degree of endogenous insulin secretion. Post hoc analyses, small observational studies, and emerging type 1 diabetes trials suggest that incretin-based therapies can improve glycemia and body weight in selected patients. These findings do not establish durable preservation of beta-cell function or justify replacing necessary insulin. Reported ketoacidosis episodes frequently involve insulin withdrawal, reduced carbohydrate intake, vomiting, dehydration, concomitant sodium–glucose cotransporter-2 inhibitors, or interrupted insulin delivery. Case reports and pharmacovigilance signals cannot establish an independent causal effect of GLP-1RAs. Before treatment escalation, clinicians should reconsider diabetes classification when the clinical course suggests insulin deficiency, maintain adequate insulin replacement, and provide individualized monitoring and sick-day guidance. Persistent gastrointestinal symptoms warrant assessment for ketosis even when glucose concentrations are not markedly elevated.
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G et al. (2026) studied this question.
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