Insulin Deintensification After Glucagon-Like Peptide-1 (GLP-1)-Based Therapy in Type 2 Diabetes: Evidence and a Practical Clinical Framework

Glucagon-like peptide-1 (GLP-1)-based therapies have changed the management of insulin-treated type 2 diabetes by creating opportunities not only to improve glycemic control and body weight but also to reduce insulin exposure and simplify previously intensified treatment regimens.However, clinical guidance remains considerably clearer on when to initiate or intensify insulin than on how to safely reduce established insulin therapy after effective GLP-1-based treatment is introduced.This narrative clinical review examines evidence for insulin dose reduction, regimen simplification, prandial insulin withdrawal, and complete insulin withdrawal following initiation or intensification of GLP-1-based therapy in adults with type 2 diabetes.Randomized trials and real-world studies increasingly support simplification of complex insulin regimens, with the strongest direct evidence supporting reduction or withdrawal of prandial insulin in appropriately selected patients.Complete insulin withdrawal is achievable in some individuals but remains less extensively studied.A practical approach should distinguish basal from prandial insulin and integrate overall glycemic control with fasting and postprandial glucose patterns, hypoglycemia risk, current insulin requirements, and clinical features suggesting impaired endogenous insulin reserve.Continuous glucose monitoring or structured glucose monitoring can facilitate sequential adjustment as GLP-1-based therapy is titrated.Patients with marked hyperglycemia, previous ketosis or diabetic ketoacidosis, suspected autoimmune diabetes, or other evidence of clinically important insulin deficiency require greater caution.We propose an evidence-informed phenotype-based framework in which insulin components are progressively reassessed rather than routinely continued or withdrawn according to a fixed formula.The objective is not insulin independence itself, but identification of the least complex insulin regimen necessary to maintain safe, individualized glycemic control.