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Conjugated bile acid-activated S1P receptor 2 is a key regulator of sphingosine kinase 2 and hepatic gene expression. | LitMetric

Conjugated bile acid-activated S1P receptor 2 is a key regulator of sphingosine kinase 2 and hepatic gene expression.

Hepatology

Department of Surgery, Medical College of Virginia Campus, Virginia Commonwealth University, Richmond, VA; Department of Biochemistry and Molecular Biology, Medical College of Virginia Campus, Virginia Commonwealth University, Richmond, VA; Division of Digestive and General Surgery, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.

Published: April 2015

AI Article Synopsis

  • Bile acids play a crucial role in managing nutrient metabolism during the feed/fast cycle by activating specific signaling pathways in liver cells, particularly through S1PR2.
  • Feeding mice a high-fat diet or manipulating S1PR2 expression affects the levels of sphingosine kinase 2 (SphK2), which is important for liver function.
  • Mice lacking S1PR2 or SphK2 experienced rapid fatty liver development on a high-fat diet, indicating that these components are essential for maintaining healthy lipid metabolism in the liver.

Article Abstract

Unlabelled: Bile acids are important hormones during the feed/fast cycle, allowing the liver to coordinately regulate nutrient metabolism. How they accomplish this has not been fully elucidated. Conjugated bile acids activate both the ERK1/2 and AKT signaling pathways via sphingosine 1-phosphate receptor 2 (S1PR2) in rodent hepatocytes and in vivo. Here, we report that feeding mice a high-fat diet, infusion of taurocholate into the chronic bile fistula rat, or overexpression of the gene encoding S1PR2 in mouse hepatocytes significantly upregulated hepatic sphingosine kinase 2 (SphK2) but not SphK1. Key genes encoding nuclear receptors/enzymes involved in nutrient metabolism were significantly downregulated in livers of S1PR2(-/-) and SphK2(-/-) mice. In contrast, overexpression of the gene encoding S1PR2 in primary mouse hepatocytes differentially increased SphK2, but not SphK1, and mRNA levels of key genes involved in nutrient metabolism. Nuclear levels of sphingosine-1-phosphate, an endogenous inhibitor of histone deacetylases 1 and 2, as well as the acetylation of histones H3K9, H4K5, and H2BK12 were significantly decreased in hepatocytes prepared from S1PR2(-/-) and SphK2(-/-) mice.

Conclusion: Both S1PR2(-/-) and SphK2(-/-) mice rapidly developed fatty livers on a high-fat diet, suggesting the importance of conjugated bile acids, S1PR2, and SphK2 in regulating hepatic lipid metabolism.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4376566PMC
http://dx.doi.org/10.1002/hep.27592DOI Listing

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