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Glucagon-like peptide-1 receptor signaling modifies the extent of diabetic kidney disease through dampening the receptor for advanced glycation end products-induced inflammation. | LitMetric

Glucagon-like peptide-1 receptor signaling modifies the extent of diabetic kidney disease through dampening the receptor for advanced glycation end products-induced inflammation.

Kidney Int

Department of Diabetes, Monash University, Central Clinical School, Alfred Research Alliance, Melbourne, Victoria, Australia; Diabetes Complications Division, Baker Heart & Diabetes Institute, Melbourne, Victoria, Australia; Drug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Monash University Parkville Campus, Parkville, Victoria, Australia. Electronic address:

Published: January 2024

AI Article Synopsis

  • GLP-1 is a hormone released after meals that has kidney-protective effects, but the mechanisms behind this are not fully understood.
  • Research found that mice without GLP-1 receptors had worse kidney issues that worsened with diabetes, but improving these effects was possible by also removing RAGE, a protein linked to inflammation and kidney damage.
  • The diabetes drug liraglutide activated GLP-1 receptors, leading to reduced inflammation and kidney damage, as well as changes in kidney cell function, suggesting that GLP-1 therapies can protect kidneys in diabetic conditions beyond their effect on blood sugar.

Article Abstract

Glucagon like peptide-1 (GLP-1) is a hormone produced and released by cells of the gastrointestinal tract following meal ingestion. GLP-1 receptor agonists (GLP-1RA) exhibit kidney-protective actions through poorly understood mechanisms. Here we interrogated whether the receptor for advanced glycation end products (RAGE) plays a role in mediating the actions of GLP-1 on inflammation and diabetic kidney disease. Mice with deletion of the GLP-1 receptor displayed an abnormal kidney phenotype that was accelerated by diabetes and improved with co-deletion of RAGE in vivo. Activation of the GLP-1 receptor pathway with liraglutide, an anti-diabetic treatment, downregulated kidney RAGE, reduced the expansion of bone marrow myeloid progenitors, promoted M2-like macrophage polarization and lessened markers of kidney damage in diabetic mice. Single cell transcriptomics revealed that liraglutide induced distinct transcriptional changes in kidney endothelial, proximal tubular, podocyte and macrophage cells, which were dominated by pathways involved in nutrient transport and utilization, redox sensing and the resolution of inflammation. The kidney-protective action of liraglutide was corroborated in a non-diabetic model of chronic kidney disease, the subtotal nephrectomised rat. Thus, our findings identify a novel glucose-independent kidney-protective action of GLP-1-based therapies in diabetic kidney disease and provide a valuable resource for exploring the cell-specific kidney transcriptional response ensuing from pharmacological GLP-1R agonism.

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Source
http://dx.doi.org/10.1016/j.kint.2023.09.029DOI Listing

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