Exploring alpha7-nicotinic acetylcholine receptors (a7R) as a type 1 diabetes therapeutic target

Presenter's Name(s)

Ryan Fitzpatrick

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 7R modulation may counter autoimmune diabetes progression by reducing -cell inflammation and restoring function. No human safe 7R compounds have yet been tested for -cell survival activity. Here we show that the 7R 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

Life Sciences

Abstract only.

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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 7R modulation may counter autoimmune diabetes progression by reducing -cell inflammation and restoring function. No human safe 7R compounds have yet been tested for -cell survival activity. Here we show that the 7R 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.