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Title: GLP-1 receptor agonist as adjuvant therapy in type 1 diabetes: No apparent benefit for Beta-cell function or glycemia

Author
item REDONDO, MARIA - Baylor College Of Medicine
item BACHA, FIDA - Children'S Nutrition Research Center (CNRC)

Submitted to: Journal of Clinical Endocrinology and Metabolism
Publication Type: Other
Publication Acceptance Date: 6/1/2020
Publication Date: 6/2/2020
Citation: Redondo, M.J., Bacha, F. 2020. GLP-1 receptor agonist as adjuvant therapy in type 1 diabetes: No apparent benefit for Beta-cell function or glycemia. Journal of Clinical Endocrinology and Metabolism. 105(8):e3000-e3002. https://doi.org/10.1210/clinem/dgaa314.
DOI: https://doi.org/10.1210/clinem/dgaa314

Interpretive Summary: Type 1 diabetes is an autoimmune disease that results in destruction of the insulin producing cells in the pancreas. This leads to rapid loss of insulin production and need for insulin therapy. New treatments are desirable to slow down this process. In this editorial, we reviewed the evidence in the literature and commented on research that evaluated the use of a new class of medication called GLP-1 receptor agonists (GLP-1RA) that work by stimulating insulin secretion. The reviewed research found no significant difference for measures of insulin secretion and other important glucose related outcomes in young adults with autoimmune diabetes who received the intervention as compared with those who did not over one year of the study. Overall the evidence with the use of these agents in individuals with type 1 diabetes does not support a significant benefit in preventing the deterioration of insulin production. However, more research is needed to determine if a subset of individuals with type 1 diabetes who have obesity or cardiovascular disease risk factors may benefit from this class of therapy.

Technical Abstract: Autoimmune type 1 diabetes (T1D) is characterized by a relatively rapid decline in beta-cell function. However, the degree and rate of beta-cell loss after clinical diagnosis varies among individuals. In individuals with T1D, greater residual beta-cell function is associated with better health outcomes, such as lower hemoglobin A1c (HbA1c) and a lower risk of diabetic complications (1). In addition, strategies that succeed at preserving beta-cell function after onset could be tried in at-risk individuals to prevent the progression to clinical disease. Therefore, there is great interest in finding treatments that lessen the loss of beta-cell function after T1D diagnosis.