Apolipoprotein CIII is a new player in diabetes. Issue 1 (February 2017)

• Record Type: Journal Article
• Authors: Juntti-Berggren, Lisa; Berggren, Per-Olof
• Is Part Of: Current opinion in lipidology. Volume 28:Issue 1(2017:Feb.)
• Page Start: 27
• Page End: 31
• Publication Date: 2017-02
• Subjects: apolipoprotein CIII -- cytoplasmic free Ca2+ concentration ([Ca2+]i) -- diabetes -- insulin resistance; Lipids -- Periodicals; 572.574
• DOI: 10.1097/MOL.0000000000000372
• Languages: English
• ISSNs: 1473-6535

Abstract

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 Ca 2+ -handling by activating voltage-gated Ca 2+ -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 Ca 2+ -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 β-cell and thereby promote the development of diabetes. Increased levels of this apolipoprotein affects intracellular Ca 2+ -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 β-cell dysfunction. Hence, targeting apoCIII may constitute a novel pharmacological strategy to treat both type-1 and type-2 diabetes.