Why the study?
No primary, secondary, or tertiary prevention or treatment is available for type-1 diabetes despite its increasing global prevalence.
This review highlights the potential role of apolipoprotein CIII in the pathogenesis of type-1 diabetes through inflammation and autoimmunity.
No T1D prevention or treatment available; leaves open need for targeted trials in autoimmune diabetes.
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.
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Valladolid‐Acebes et al. (2021) studied this question.
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