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Suh, Pann-Ghill
BioSignal Network Lab (BSN)
Research Interests
  • Signal transduction, cancer, metabolism, phospholipase C


Lysophosphatidylserine regulates blood glucose by enhancing glucose transport in myotubes and adipocytes

DC Field Value Language Yea, Kyungmoo ko Kim, Jaeyoon ko Lim, Seyoung ko Kwon, Taewan ko Park, Ho Seon ko Park, Kyong Soo ko Suh, Pann-Ghill ko Ryu, Sung Ho ko 2014-09-04T00:40:26Z - 2014-09-03 ko 2009-01 ko
dc.identifier.citation BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.378, no.4, pp.783 - 788 ko
dc.identifier.issn 0006-291X ko
dc.identifier.uri -
dc.description.abstract Lysophosphatidylserine (LPS) is known to have diverse cellular effects, but although LPS is present in many biological fluids, its in vivo effects have not been elucidated. In the present study, we investigated the effects of LPS on glucose metabolism in vivo, and how skeletal muscle cells respond to LPS stimulation. LPS enhanced glucose uptake in a dose- and time-dependent manner in L6 GLUT4myc myotubes, and this effect of LPS on glucose uptake was mediated by a Gαi and PI 3-kinase dependent signal pathway. LPS increased the level of GLUT4 on the cell surface of L6 GLUT4myc myotubes, and enhanced glucose uptake in 3T3-L1 adipocytes. In line with its cellular functions, LPS lowered blood glucose levels in normal mice, while leaving insulin secretion unaffected. LPS also had a glucose-lowering effect in STZ-treated type 1 diabetic mice and in obese db/db type 2 diabetic mice. This study shows that LPS-stimulated glucose transport both in skeletal muscle cells and adipocytes, and significantly lowered blood glucose levels both in type 1 and 2 diabetic mice. Our results suggest that LPS is involved in the regulation of glucose homeostasis in skeletal muscle and adipose tissue. ko
dc.description.statementofresponsibility close -
dc.language 영어 ko
dc.title Lysophosphatidylserine regulates blood glucose by enhancing glucose transport in myotubes and adipocytes ko
dc.type ARTICLE ko
dc.identifier.scopusid 2-s2.0-57849114292 ko
dc.identifier.wosid 000262447400019 ko
dc.type.rims ART ko
dc.description.wostc 10 *
dc.description.scopustc 9 * 2015-05-06 * 2014-09-03 *
dc.identifier.doi 10.1016/j.bbrc.2008.11.122 ko
dc.identifier.url ko
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