Abstract
It is well known that type-2 diabetes mellitus (T2D) is increasing worldwide, but also the autoimmune form, type-1 diabetes (T1D), is affecting more people. The latest estimation from the International Diabetes Federation (IDF) is that 1.1 million children and adolescents below 20 years of age have T1D. At present, we have no primary, secondary or tertiary prevention or treatment available, although many efforts testing different strategies have been made. This review is based on the findings that apolipoprotein CIII (apoCIII) is increased in T1D and that in vitro studies revealed that healthy β-cells exposed to apoCIII became apoptotic, together with the observation that humans with higher levels of the apolipoprotein, due to mutations in the gene, are more susceptible to developing T1D. We have summarized what is known about apoCIII in relation to inflammation and autoimmunity in in vitro and in vivo studies of T1D. The aim is to highlight the need for exploring this field as we still are only seeing the top of the iceberg.
Highlights
Berggren, P.-O.; Juntti-Berggren, L.Diabetes mellitus has been known for more than 3500 years, but still there are many unanswered questions
It has been established for many years that there is a relationship between apolipoprotein CIII (apoCIII) and cardiovascular diseases (CVDs) [55,56,57,58,59]; the nature of this is due to modulations in lipoprotein metabolism, and inflammation, which is regarded as an important part of the development of atherosclerosis
Changes in [Ca2+ ]i are playing a major role for the stimulus-secretion coupling leading to secretion of insulin from the β-cells, and the apoCIII-mediated hyperactivation of the voltage-gated Ca2+ channels resulted in apoptosis that could be prevented by a Ca2+ channel blocker [20,81]
Summary
Nearly two decades later, it was shown that the kinetics of the isoforms apoCIII1 and CIII2 show the strongest correlation to hypertriglyceridemia and reduced VLDL, intermediatedensity lipoproteins (IDLs) and apoB-100 catabolism, which are important risk factors for cardiovascular diseases (CVDs) [17]. The main pathways by which apoCIII exerts its actions are the inhibition of lipoprotein lipase (LPL)-mediated lipolysis and the prevention of the hepatic clearance of TRL via the LDL receptor (LDLR) and LDL-related protein 1 (LRP1) [27,28,29,30,31,32]. Both mechanisms are tightly related since the clearance of circulating triglycerides (Tgs) is linked to lipolysis of TRLs by LPL [27,28,29,30,31,32]
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