Novel Leptin-Islet Signaling Pathway Regulates Beta Cell Function and Proliferation
Abstract
This proposal addresses the Fiscal Year 2022 Peer Reviewed Medical Research Program Topic Area of Diabetes. Type 2 diabetes (T2D) has become a global health pandemic that greatly shortens lifespan and carries a significant economic burden. U.S. Veterans are particularly susceptible, developing T2D three times more often than the general population. There is a significant need for new treatments in T2D, especially for the U.S. Veteran community. T2D develops when the insulin-secreting beta cells of the pancreas fail to meet the body’s insulin requirements. Drugs that can increase the number of functioning beta cells represent strong candidates to treat T2D; however, no such drugs are currently available, creating a critical unmet need in the medical community. The satiety hormone leptin can suppress the ability of beta cells to function and grow. In contrast, blocking leptin effects on beta cells can dramatically increase the number of beta cells. The mechanism is yet to be defined, but we hypothesize that leptin acts on nearby delta cells that secrete an inhibitory hormone, somatostatin, to suppress beta cells. This is an innovative concept that will describe for the first time the effects of leptin on human delta cells and define the mechanism regulating beta cell function and growth. Furthermore, this proposal represents a conceptual shift in how leptin activity outside of the brain can significantly impact metabolism and pancreatic beta cells. This proposal will address the strategic goal to understand correlations between nutrition and metabolic disease susceptibility. Ultimately, these studies will reveal new drug targets to increase the number of functioning beta cells to overcome T2D.
Document Details
- Document Type
- DoD Grant Award
- Publication Date
- Jan 04, 2024
- Source ID
- HT94252310113
Entities
People
- Richard M Cox
Organizations
- Baylor College of Medicine
- United States Army