Pancreatic hypersecretion of amyloid-forming human amylin dysregulates the neuro-immune axis and B cell development in a model of type-2 diabetes.

ABSTRACT: During Type 2 diabetes (T2D), the immune system becomes dysregulated, adopting a pro-inflammatory phenotype and secreting cytokines that exacerbate inflammation. Human amylin (i.e., islet amyloid polypeptide) secreted from the pancreas of HIP rats during T2D has been shown to deposit in the microvasculature and lead to neurodegeneration and cognitive decline. Although T2D is linked to neuroinflammation and cognitive impairment, whether and how peripheral immune changes, driven in part by amyloidogenic amylin deposition, shape these outcomes is not well understood. We investigated how the accumulation of pancreatic human amylin impacts the peripheral and neuroimmune response in transgenic rat and mouse models with endogenous overexpression. In rats, hypersecretion of pancreatic human amylin

SUBMITTER: Winford ED 

PROVIDER: S-EPMC12609684 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature