Abstract
Biomarkers are important tools for describing the adequacy or inadequacy of biological processes (to allow for the early and accurate diagnosis) and monitoring the biological effects of intervention strategies (to identify and develop optimal dose and treatment strategies). A number of lipid biomarkers are implicated in metabolic disease and the circulating levels of these biomarkers are used in clinical settings to predict and monitor disease severity. There is convincing evidence that specific circulating ceramide species can be used as biological predictors and markers of cardiovascular disease, atherosclerosis and type 2 diabetes mellitus. Here, we review the existing literature that investigated sphingolipids as biomarkers for metabolic disease prediction. What are the advantages and disadvantages? Are circulating ceramides predominantly produced in the liver? Will hepatic sphingolipid inhibitors be able to completely prevent and treat metabolic disease? As sphingolipids are being employed as biomarkers and potential metabolic disease treatments, we explore what is currently known and what still needs to be discovered.
Highlights
The escalating epidemic of obesity and its metabolic co-morbidities such as type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD) are major sources of adverse health effects, impaired quality of life and morbidity [1]
Being overweight or obese is one of the major underlying factors that contributes to T2DM and if left unchecked, T2DM can contribute to a higher risk of CVD events
The most recent of these circulating factors is a group of sphingolipids that have been associated with both CVD and T2DM in a number of metabolic disease studies
Summary
The escalating epidemic of obesity and its metabolic co-morbidities such as type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD) are major sources of adverse health effects, impaired quality of life and morbidity [1]. The most recent of these circulating factors is a group of sphingolipids that have been associated with both CVD and T2DM in a number of metabolic disease studies. The addition of the unique fatty acid to a sphingoid backbone, results in the generation of highly specific ceramide species (CerS1 for C18:0 ceramides, CerS2 for C22:0-C24:0, CerS4 for C18:0-C20:0, CerS5 and CerS6 for C16:0) demonstrating CerSs are paramount for exclusive ceramide manipulation [5, 14, 19,20,21] This is evident as targeting CerS6 to reduce C16:0 ceramides, resulted in the prevention of diet-induced obesity and glucose intolerance [14, 16], whilst the ablation of CerS2 reduced C22:0 and C24:0 ceramides, increased C16:0 ceramides and contributed to spontaneous hepatocellular carcinoma development [18]. This is especially important since it is not always the most predominant ceramide species or CerS enzyme that can have the most detrimental effect
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