Abstract
Purpose of review
Type-1 and type-2 diabetes are diseases with an increasing number of patients and a complex, multifactorial pathogenesis. Apolipoprotein (apo) CIII is increased in both types of diabetes and interventions preventing the increase have effects on the development of diabetes.
Recent findings
ApoCIII affects intracellular Ca2+-handling by activating voltage-gated Ca2+-channels. ApoCIII is produced within the pancreatic islets and it increases in parallel with the development of insulin resistance and type-2 diabetes. Preventing the increase maintains a normal glucose tolerance as well as Ca2+-handling and no signs of inflammation can be seen in islets wherein the augmented local production of the apolipoprotein is absent.
Summary
ApoCIII has been found to interfere with both function and survival of the beta-cell and thereby promote the development of diabetes. Increased levels of this apolipoprotein affects intracellular Ca2+-handling and insulin sensitivity, which finally results in impaired glucose homeostasis and diabetes. Interestingly, in a type-1 diabetes rat model lowering of apoCIII delays onset of diabetes. In type-2 diabetes insulin resistance within the pancreatic islets leads to a local increase in apoCIII that promotes inflammation and beta-cell dysfunction. Hence, targeting apoCIII may constitute a novel pharmacological strategy to treat both type-1 and type-2 diabetes.
