Exploring alpha7-nicotinic acetylcholine receptors (a7R) as a type 1 diabetes therapeutic target
Conference Year
2023
Abstract
Type 1 diabetes involves the immune-mediated destruction of pancreatic ß-cells, the body's sole source of insulin. Besides insulin and its formulations, no widely accessible treatments or preventative therapies are available. Based on our prior animal studies, systemic α7R modulation may counter autoimmune diabetes progression by reducing ß-cell inflammation and restoring function. No human safe α7R compounds have yet been tested for ß-cell survival activity. Here we show that the α7R partial agonist GTS-21 exhibits both STAT3-dependent anti-inflammatory activity and CREB/Akt-driven survival signaling in rat INS-1 cells. Thus, GTS-21 may be suitable for further testing for anti-diabetes activity in mouse models
Primary Faculty Mentor Name
Tom Jetton
Status
Undergraduate
Student College
College of Arts and Sciences
Program/Major
Biochemistry
Primary Research Category
Arts & Humanities
Exploring alpha7-nicotinic acetylcholine receptors (a7R) as a type 1 diabetes therapeutic target
Type 1 diabetes involves the immune-mediated destruction of pancreatic ß-cells, the body's sole source of insulin. Besides insulin and its formulations, no widely accessible treatments or preventative therapies are available. Based on our prior animal studies, systemic α7R modulation may counter autoimmune diabetes progression by reducing ß-cell inflammation and restoring function. No human safe α7R compounds have yet been tested for ß-cell survival activity. Here we show that the α7R partial agonist GTS-21 exhibits both STAT3-dependent anti-inflammatory activity and CREB/Akt-driven survival signaling in rat INS-1 cells. Thus, GTS-21 may be suitable for further testing for anti-diabetes activity in mouse models