Gestational diabetes triggers postpartum cardiac hypertrophy via activation of calcineurin/NFAT signaling.

Population-based studies identified an association between a prior pregnancy complicated by gestational diabetes mellitus (GDM) and cardiac hypertrophy and dysfunction later in life. It is however unclear whether GDM initiates this phenotype and what are the underlying mechanisms. We addressed these questions by using female rats that express human amylin (HIP rats) as a GDM model and their wild-type (WT) littermates as the normal pregnancy model.

Amylin and diabetic cardiomyopathy - amylin-induced sarcolemmal Ca leak is independent of diabetic remodeling of myocardium.

Amylin is a pancreatic β-cell hormone co-secreted with insulin, plays a role in normal glucose homeostasis, and forms amyloid in the pancreatic islets of individuals with type-2 diabetes. Aggregated amylin is also found in blood and extra-pancreatic tissues, including myocardium. Myocardial amylin accumulation is associated with myocyte Ca dysregulation in diabetic rats expressing human amylin.