Abstract

Chronically elevated blood sugar, a pathological hallmark of type 2 diabetes, increases the risk for stroke and heart disease. While we know that our genetics play a significant role in who develops diabetes, scientists still do not understand the “how” behind many of the genes linked to the disease. This project aims at solving one of these genetic mysteries to uncover new ways to treat and prevent diabetes.

The research focuses on a specific protein called SLC16A13. Previous large-scale genetic studies have shown that variations in the SLC16A13 gene are strongly linked to an increased risk of diabetes, but until now, the actual function of SLC16A13 was unknown. Preliminary research shows that SLC16A13 acts as a “cellular doorway” or transporter that moves vitamin B5 (pantothenate) out of cells. This is critical because vitamin B5 is the essential building block for Coenzyme A (CoA), a molecule that acts as a master controller for how the liver produces sugar. When this “doorway” does not function correctly, vitamin B5 builds up inside liver cells, leading to an overabundance of CoA. This may cause the liver to pump out excessive amounts of sugar into the bloodstream.

The present project will (1) characterize the structure and function of the SLC16A13 transporter, and (2) study the diabetes link using well-established mouse and cell models.

In conclusion, this project studies SLC16A13 as a regulator of blood glucose, providing a clear roadmap for developing new drugs that may be able to stop the liver from producing excess sugar in diabetes.