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Discovering A New Target for Diabetes Treatment
Discovering A New Target for Diabetes Treatment

Diabetes, the seventh leading cause of death in the US, is a chronic illness that affects over 37 million Americans. In type 2 diabetes, the most common form of the disease, the hormone insulin does not remove enough glucose (sugar) from the bloodstream leading to higher-than-normal levels of glucose in the blood. This can lead to heart disease, kidney failure, and vision loss over time. There are, however, hormones other than insulin that can lower blood glucose, including GLP-1, which is produced by cells of the intestine. A family of proteins, called G protein-coupled receptors (GPCRs), regulate GLP-1. This knowledge spurred researchers from the Common Fund’s Illuminating the Druggable Genome (IDG) program to investigate the potential of GPRCs in the development of new therapies for type 2 diabetes.

A major goal of the IDG program is to discover information about members of the GPCR protein family that are not well-studied. Dr. Hongxia Ren and colleagues sought to learn more about one such GPCR, Gpr17. Using samples from human and rodent intestinal tissue, the researchers found that Gpr17 tends to co-occur in cells where the hormone GLP-1 is produced. This led the study team to explore the effect of removing Gpr17 on blood glucose. They discovered that when Gpr17 functionality was removed from mouse models, the mice’s ability to lower blood glucose increased. Further, using a 3D model of the intestine derived from mice without Gpr17, the researchers found an increase in the secretion of GLP-1. Though more research is needed, this study demonstrates that Gpr17 has a role in regulating blood glucose and could serve as a new drug target for patients with uncontrolled type 2 diabetes.


Intestinal Gpr17 deficiency improves glucose metabolism by promoting GLP-1 secretion. S. Yan, J.M. Conley, A.M. Reilly, N.D. Stull, S.D. Abhyankar, A.C. Ericsson, T. Kono, A.I. Molosh, C.A. Kubal, C. Evans-Molina, H. Ren. Cell Rep. 2022 Jan 4; 38(1):5449.

This page last reviewed on August 24, 2023