Inflammation, Diabetes, and the Pancreas

Q & A with Anna Casu, MD, AdventHealth Translational Research Institute, Associate Investigator

The pancreas is a vital organ that plays a dual role in the body. As part of the digestive system, it produces enzymes essential for breaking down food. Simultaneously, it functions as an endocrine organ, secreting hormones like insulin and glucagon that regulate blood sugar levels. Insulin is crucial for the transport of glucose from the bloodstream into cells for energy. Diabetes occurs when the pancreas doesn't produce enough insulin (Type 1 diabetes) or when the amount of insulin produced is insufficient the body becomes resistant to insulin (Type 2 diabetes), leading to elevated blood sugar levels.

Q: Will you elaborate on the significance of the Pancreas Fest in the field of pancreatic research?

Dr. Casu: The Pancreas Fest is crucial as it has filled a significant gap in the research community by solely focusing on the often-overlooked exocrine pancreas. This dedicated platform has fostered collaboration and knowledge sharing among researchers, clinicians, and other professionals, leading to advancements in our understanding of exocrine pancreas diseases and their relationship to the endocrine pancreas.

Q: How has the focus of the Pancreas Fest evolved over the years?

Dr. Casu: Initially, the conference primarily centered on exocrine pancreas diseases. However, as the understanding of the intricate connection between the exocrine and endocrine functions of the pancreas has grown, the Pancreas Fest has expanded its scope to include discussions on their interplay. This evolution reflects the increasing recognition of the importance of a holistic approach to pancreatic research.

Q: What are the potential mechanisms by which inflammation contributes to diabetes development in pancreatitis patients?

Dr. Casu: Inflammation is believed to play a pivotal role in the development of diabetes following pancreatitis. One potential mechanism is the disruption of insulin secretion caused by inflammatory mediators. Additionally, inflammation may contribute to the autoimmune process leading to beta cell destruction, although more research is needed to fully elucidate this connection.

Q: How does the T1D and Acute Pancreatitis Consortium aim to differentiate between Type 1 and Type 2 diabetes mechanisms in this population?

Dr. Casu: The consortium's comprehensive approach to distinguishing between Type 1 and Type 2 diabetes mechanisms, or other yet unknown mechanisms, in the context of pancreatitis, holds great promise. By collecting detailed clinical data, genetic information, and various biological samples, researchers can identify specific biomarkers and pathways associated with each type of diabetes. This knowledge, when applied, will be instrumental in developing targeted therapies and prevention strategies, offering hope for improved outcomes in pancreatic diseases.

Q: Explain in more detail the potential role of stellate cells in both Type 1 diabetes and pancreatitis?

Dr. Casu: Stellate cells are primarily known for their involvement in fibrosis. However, emerging evidence suggests a broader role in pancreatic diseases. In Type 1 diabetes, these cells may contribute to beta cell loss through inflammatory processes or by interfering with insulin production. My laboratory investigates these aspects in detail by studying human cells. In pancreatitis, their role in fibrosis and potential impact on insulin production are areas of active investigation.

Q: How does your research on adipose tissue infiltration of the pancreas complement your work on stellate cells?

Dr. Casu: Adipose tissue infiltration and stellate cells are probably interconnected. Both factors seem to contribute to pancreatic dysfunction. By studying these processes together, we can gain a more comprehensive understanding of the mechanisms underlying pancreatitis and diabetes. Additionally, targeting these pathways may offer novel therapeutic opportunities.

Q: How can your research be expanded to deepen our understanding of the exocrine-endocrine pancreas interaction?

Dr. Casu: To deepen our understanding of the exocrine-endocrine pancreas interplay, future research will focus on identifying specific molecular and cellular mechanisms driving this interaction. Additionally, exploring the role of the gut microbiome in modulating pancreatic function is a promising avenue. Ultimately, these findings will inform the development of targeted therapies to prevent and treat pancreatic diseases.

Q: How do you envision the field of pancreatic research evolving in the next decade?

Dr. Casu: The field of pancreatic research is poised for significant advancements due to technological breakthroughs and increased collaboration. We can anticipate a deeper understanding of the genetic and environmental factors contributing to pancreatic diseases. Furthermore, personalized medicine approaches will become increasingly prevalent, allowing for tailored treatment strategies based on individual patient characteristics.

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