We read with great interest the study by Amendolara et al. (1), which showed that individuals with latent autoimmune diabetes in adults (LADA) have lower C-peptide levels than BMI-, sex-, and disease duration–matched individuals with type 2 diabetes across comparable levels of estimated insulin resistance. The finding that C-peptide tracked insulin resistance indexes in type 2 diabetes but not in LADA provides an important physiological explanation for why adult-onset autoimmune diabetes may not follow the usual compensatory β-cell response pattern.
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