Abstract
Apolipoprotein M (apoM) is a member of the lipocalin superfamily and an important carrier of the small bioactive lipid sphingosine-1-phosphate (S1P). The apoM/S1P complex is attached to all lipoproteins, but exhibits a significant preference for high-density lipoproteins. Although apoM, S1P, and the apoM/S1P complex have been discovered more than a decade earlier, the overall function of the apoM/S1P complex remains controversial. Evidence suggests that the complex plays a role in inflammation and cholesterol metabolism and is important for maintaining a healthy endothelial barrier, regulating the turnover of triglycerides from lipoproteins, and reducing cholesterol accumulation in vessel walls. Recent studies have also addressed the role of apoM and S1P in the development of diabetes and obesity. However, limited evidence is available, and the data published so far deviates. This review discusses the specific elements indicative of the protective or harmful effects of apoM, S1P, and the apoM/S1P complex on type 2 diabetes development. Since drugs targeting the S1P system and its receptors are available and could be potentially used for treating diabetes, this research topic is a pertinent one.
Highlights
Apolipoprotein M was discovered in 1999 [1] and has since been associated with various conditions, such as atherosclerosis, cardiovascular disease [2], dyslipidemia [3], diabetes [4, 5], inflammation, and sepsis [6]
Based on the observation that changes in signaling via the S1Preceptors in animal models can delay the development of diabetes, and that plasma Apolipoprotein M (apoM) levels may be used as a subclassification marker in humans, studies addressing the role of genetic changes in apoM and its association with increased risk of diabetes were performed
As a biomarker for diabetes, it is likely that plasma apoM can be used to distinguish between patients with MODY3 and T1D but not T2D
Summary
Apolipoprotein M (apoM) was discovered in 1999 [1] and has since been associated with various conditions, such as atherosclerosis, cardiovascular disease [2], dyslipidemia [3], diabetes [4, 5], inflammation, and sepsis [6]. These models lack control of food consumption, which leads to an increase in the body weight and plasma insulin, with the potential risk of insulin resistance development, resembling obesity in humans Both ob/ ob and db/db mice showed a significant reduction in plasma apoM levels (approximately 30%–50%) [35]. Based on the observation that changes in signaling via the S1Preceptors in animal models can delay the development of diabetes, and that plasma apoM levels may be used as a subclassification marker in humans, studies addressing the role of genetic changes in apoM and its association with increased risk of diabetes were performed. The study reported a higher frequency of the C724-del allele in patients with T2D than
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
