Pancreatic islet remodeling in horses with hyperinsulinemia and pituitary dysfunction.

The equine pancreas remains understudied, particularly in the context of endocrine disease. This study aimed to characterize regional islet distribution and composition in the normal equine pancreas and investigate how hyperinsulinemia (HI) and pituitary pars intermedia dysfunction (PPID) influence pancreatic islet morphology and hormone expression. In the first experiment, pancreas samples from eight healthy horses were collected and analyzed across three anatomical locations: left lobe, body, and right lobe. The left lobe exhibited a greater relative islet area and perimeter compared to the body and right lobe, though islet composition remained consistent with a similarly proportional alpha-cell core, beta-cell mantle, and scattered delta-cells. In the second experiment, pancreas tissues from thirty-five horses with defined endocrine disease status were evaluated. HI was associated with larger islets and greater insulin immunostaining, while PPID was associated with increased islet number without changes in islet size or insulin immunostaining, suggesting divergent disease-specific adaptations. Findings support the hypothesis that HI drives islet expansion as a compensatory response to insulin resistance, whereas PPID promotes islet neogenesis. The observed increase in islet number in PPID horses may reflect a previously unrecognized mechanism influenced by chronic endocrine stimulation. These results established foundational knowledge of normal equine islet architecture and highlight the dynamic adaptability of the endocrine pancreas in response to metabolic and pituitary disorders.