|

Estimated Read Time:

2–3 minutes

Presenter Profile: Modeling Exocrine-Endocrine Cross Talk

Ridhdhi Desai, PhD

Assistant Professor
Drexel University

Featured in the Session: The Pancreatic Ecosystem: How Exocrine Tissue Orchestrates Islet Biology

When

Monday, June 8
at 8:00 a.m.

Where

355 (Level 3)
Ernest N. Morial Convention Center

Ridhdhi Desai, PhD
Ridhdhi Desai, PhD

What is your presentation about?

Understanding pathogenesis and progression of pancreatic diseases, which often entails abnormalities within the exocrine cells, continues to be a challenge given the difficulties associated with (1) accessing pancreatic tissue from living patients; (2) isolating adequate numbers of high-quality ductal and acini cells that are amenable to in vivo and ex vivo experiments; and (3) lack of mouse models that fully recapitulate effects observed in human patients. These limitations are especially evident at the level of understanding how interactions between different cell types within the pancreatic tissue contribute to progression of pancreatic diseases, specifically in the context of diabetes and pancreatic cancer. This talk will present development of human stem-cell derived pancreatic organoid models to identify exocrine-associated abnormalities and the complicated interplay between exocrine and endocrine cells that influence beta cell function during disease progression.

How do you hope your presentation will impact diabetes research or care?

In the United States, type 1 diabetes, an autoimmune disease, affects approximately 2 million individuals, and is predicted to grow over the next few decades. At early stages of disease onset, prior to clinical diagnosis and perhaps even before the development of islet autoimmunity, individuals with type 1 diabetes have smaller pancreases, reduced number of pancreatic acini, decreased secretion of exocrine enzymes, and increased fibrosis. This suggests that type 1 diabetes is likely a disorder of both exocrine and endocrine pancreas, and that exocrine damage can act as a potential trigger for beta cell dysfunction in type 1 diabetes. Using our human stem-cell derived exocrine model, we hope to understand interactions between exocrine and endocrine cells and how they contribute to the development and progression of type 1 diabetes. Ultimately, I hope to utilize the knowledge gained for development of biomarkers and therapies that allow regeneration, protection, or restoration of beta cells during disease progression.

How did you become involved with this area of diabetes research or care?

I completed my postdoctoral training at both Beth Israel Deaconess Medical Center (Dr. Senthil Muthuswamy) and Joslin Diabetes Center/Harvard Medical School (Dr. Rohit Kulkarni), and since 2023, I am an assistant professor at Drexel University, department of biochemistry and molecular biology. My research focuses on using human stem-cell derived pancreatic ductal and acini organoids to study how cell lineage tropism regulates fundamental mechanisms associated with the pathogenesis of pancreatic diseases; and whether exocrine-specific abnormalities influence normal beta cell function during disease progression, specifically in the context of type 1 diabetes and pancreatic cancer.