JOURNAL ARTICLE
REVIEW
Add like
Add dislike
Add to saved papers

Sphingosine 1-phosphate in metabolic syndrome (Review).

Metabolic syndrome (MetS), a clustering of components, is closely associated with the development and prognosis of cardiovascular disease and diabetes. Sphingosine 1-phosphate (S1P) is a lysophospholipid with paracrine and autocrine effects, which is associated with obesity, insulin resistance, hyperglycemia, dyslipidemia and hypertension through extracellular and intracellular signals to achieve a variety of biological functions. However, there is controversy regarding the role of S1P in MetS; the specific role played by S1P remains unclear. It ameliorates abnormal energy metabolism and deviant adipogenesis and mediates inflammation in obesity. Despite the fact that sphingosine kinase (SphK)2/S1P increases the glucose‑stimulated insulin secretion of β-cells, more evidence showed that activation of the SphK1/S1P/S1P2R pathway inhibited the feedback loop of insulin secretion and sensitivity. The majority of S1P1R activation improves diabetes whereas S1P2R activation worsens the condition. In hyperlipidemia, S1P binds to high-density lipoprotein, low‑density lipoprotein and very low-density lipoprotein exerting different effects. Moreover, low concentrations of S1P lead to vasodilation whereas high concentrations of S1P result in vasocontraction of isolated arterioles. This review discusses the means by which different SphKs, S1P concentrations or S1P receptor subtypes results to diverse result in MetS, and then examines the role of S1P in MetS.

Full text links

We have located links that may give you full text access.
Can't access the paper?
Try logging in through your university/institutional subscription. For a smoother one-click institutional access experience, please use our mobile app.

For the best experience, use the Read mobile app

Mobile app image

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app

All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

By using this service, you agree to our terms of use and privacy policy.

Your Privacy Choices Toggle icon

You can now claim free CME credits for this literature searchClaim now

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app