Type 1 Diabetes Mice

Type 1 diabetes models include beta cell-specific knockouts (Insulin-Cre), spontaneous autoimmune models (NOD mice), chemically induced models (streptozotocin), and combinations. Beta cell-specific knockouts model beta cell loss, while NOD mice model autoimmune diabetes. Models can be combined for more complex disease modeling.

NOD mice develop spontaneous autoimmune diabetes through complex genetic and immunological mechanisms, modeling human autoimmune diabetes. Beta cell-specific knockouts model beta cell loss directly without autoimmune components. Both approaches have value: NOD for autoimmune mechanisms, beta cell knockouts for beta cell function studies.

Yes. Humanized HLA molecules or cytokines enable testing of human-specific therapeutics in T1D models. For example, NOD mice expressing human HLA-DR3 provide immune context for testing therapeutic antibodies targeting human immune pathways. Humanization enables preclinical testing of human-specific therapeutics.

Standard endpoints include blood glucose levels (fasting and random), glucose tolerance testing, insulin levels, islet histology (beta cell mass, insulitis), autoantibody titers, and immune cell infiltration. Disease progression can be monitored longitudinally, and animals may require insulin treatment to prevent severe hyperglycemia.

Combining beta cell-specific knockouts with autoimmune-prone backgrounds (e.g., NOD) or immune system modifications enables study of both primary beta cell dysfunction and secondary autoimmune amplification. This approach can distinguish primary effects from secondary immune responses, providing more comprehensive disease modeling. (/request-quote)