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Dr. Chad HunterDivision of Endocrinology, Diabetes, and Metabolism Associate Professor Chad Hunter, Ph.D., recently published an article exploring the role of a co-regulator, SSBP3, in pancreatic islet cell function.

A co-regulator is a protein that interacts with transcription factors and other regulatory proteins to influence gene expression. The Hunter Lab found that this particular co-regulator, SSBP3, interacts with other key pancreatic islet regulators, and hypothesized that it is required for pancreatic islet cell function.

A pancreatic islet is a cluster of hormone-producing cells in the pancreas. Of note, the beta cell (β-cell) within the islet is responsible for producing the glucose-lowering hormone, insulin. In those with Type 1 and Type 2 diabetes, β-cells are often damaged or destroyed, resulting in decreased insulin production and higher blood glucose levels.

The Hunter Lab article “The SSBP3 co-regulator is required for glucose homeostasis, pancreatic islet architecture, and beta-cell identity” was published in the peer-reviewed, scientific journal Molecular Metabolism. The first author of the study is a former Hunter Lab Ph.D. student, Eliana Toren, Ph.D.

“Almost nothing was known about the co-regulator SSBP3 and how it affects the function of β-cells, so our lab was interested in learning more about its role,” said Hunter. “Our team really went above and beyond is characterizing this co-regulator’s role in pancreatic islet cells overall.”

Ultimately, authors concluded that SSBP3 drives proper islet cell identity and function, where its loss causes altered islet-cell abundance and impaired glucose homeostasis. β-cell SSBP3 is required for insulin secretion and glucose homeostasis, at least partially through regulation of target genes shared with key interacting factors, the Ldb1 co-regulator and Islet-1 transcription factor, which the Hunter lab also has strong interest in.

The study may be an important step in understanding how beta-cells are normally developed and function, which can then give us clues about how to offset the damage or destruction of pancreatic cells during diabetes.

“Research like ours can provide key information toward an upstream approach – stopping the destruction of pancreatic cells – as well as a downstream approach – replacing pancreatic cells that were destroyed in those with diabetes,” said Hunter.

All study authors include: Eliana Toren, Ph.D., Jessica D. Kepple, Ph.D., Kristen V. Coutinho, Samuel O. Poole, Iztiba M. Deeba, Tanya H. Pierre, Yanping Liu, Ph.D., Maigen M. Bethea, Ph.D., and Chad S. Hunter, Ph.D.

Of note, this publication features all current Hunter Lab graduate trainees– Tanya Pierre, Kristen Coutinho, and Iztiba Deeba– as well as three former Ph.D. students that have accelerated into professional scientific roles across the nation­– Eliana Toren, Ph.D., Jessica Kepple, Ph.D., and Maigen Bethea, Ph.D.

“This publication was a wonderful example of collaboration across our current and former trainees,” said Hunter. “I am so pleased that this research demonstrates one of our lab’s top priorities: training the next generation of diabetes professionals.”