Latent Autoimmune Diabetes
Latent Autoimmune Diabetes - Related Videos
10:03
Bioluminescent Monitoring of Graft Survival in an Adoptive Transfer Model of Autoimmune Diabetes in Mice
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Cited by 1 •
2022
This protocol describes a straightforward and minimally invasive method for transplanting and imaging NIT-1 cells in non-obese diabetic (NOD)-severe combined immunodeficient mice challenged with splenocytes purified from spontaneously diabetic NOD mice.
16:26
Regulatory T cells: Therapeutic Potential for Treating Transplant Rejection and Type I Diabetes
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Cited by 2 •
2007
11:31
High-Efficiency Generation of Antigen-Specific Primary Mouse Cytotoxic T Cells for Functional Testing in an Autoimmune Diabetes Model
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2019
This article describes a protocol for the generation of antigen-specific CD8 T cells, and their expansion in vitro, with the aim of yielding high numbers of functional T cells for use in vitro and in vivo.
10:43
Transplantation of Pancreatic Islets Into the Kidney Capsule of Diabetic Mice
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Cited by 98 •
2007
Our protocol was developed to cleanly and easily deliver islets or cells under the kidney capsule of mice. Cells are concentrated into pellets in the final tubing used for transplanting the cells under the kidney capsule. The ease of this technique reduces stress to the cells and the mouse.
06:50
A High-Throughput Electrochemiluminescence 7-Plex Assay Simultaneously Screening for Type 1 Diabetes and Multiple Autoimmune Diseases
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Cited by 3 •
2020
We model a simple multiplexed ECL assay that combines 7 autoantibody assays together. The assay is capable of screening for T1D and multiple other autoimmune diseases, simultaneously, including celiac disease, autoimmune thyroid disease, and autoimmune polyglandular syndrome 1.
FAQs
Progressive loss of pancreatic beta-cell function means endogenous insulin secretion may become insufficient over time. A medication plan that initially controls glucose may therefore need reassessment as insulin production declines. Recognizing this trajectory helps clinicians anticipate when treatment must shift toward insulin replacement, rather than continuing to depend exclusively on therapies designed for insulin resistance.
Autoantibodies against glutamic acid decarboxylase can provide evidence that impaired glucose regulation has an autoimmune basis rather than reflecting nonautoimmune insulin resistance alone. This distinction matters pharmacologically because it signals a likely decline in endogenous insulin secretion. Incorporating antibody results into classification can reduce inappropriate reliance on glucose-lowering treatment intended primarily for insulin-resistant disease.
The central pharmacological difference is the expected direction of beta-cell function. In insulin-resistant disease, treatment may focus on improving glucose control despite preserved or emphasized insulin resistance, whereas latent autoimmune diabetes includes progressive loss of insulin production. Consequently, therapies that address insulin deficiency become increasingly important, and insulin may eventually be required for adequate glycemic control.
The key consideration is the extent and progression of endogenous insulin loss. As immune-mediated beta-cell destruction reduces the pancreas’s ability to produce insulin, glucose-lowering treatment that does not replace insulin may become inadequate. Clinicians can use the patient’s disease classification and changing glycemic control to guide medication reassessment and determine when insulin-based treatment is appropriate.
Evaluation can include testing for circulating autoantibodies, particularly antibodies against glutamic acid decarboxylase, when the clinical classification is uncertain. A positive autoimmune marker can distinguish this condition from nonautoimmune disease and prompt closer attention to declining insulin secretion. That classification supports a more appropriate pharmacological plan instead of assuming persistent insulin-resistance-focused treatment is sufficient.
Classification should influence management as soon as the possibility of autoimmune beta-cell loss is recognized, especially when an adult’s presentation resembles type 2 diabetes. Early recognition helps align medication selection with the expected decline in endogenous insulin production. In practice, this can reduce delays in appropriate insulin therapy and support more consistent glycemic control as the disease progresses.