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

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

Cited 10 times inthomson ciCited 9 times inthomson ci
Title
Lysophosphatidylserine regulates blood glucose by enhancing glucose transport in myotubes and adipocytes
Author
Yea, KyungmooKim, JaeyoonLim, SeyoungKwon, TaewanPark, Ho SeonPark, Kyong SooSuh, Pann-GhillRyu, Sung Ho
Keywords
Adipocytes; Diabetes; Glucose lowering; Glucose uptake; GLUT4; Insulin; Lysophosphatidylserine; Myotubes
Issue Date
200901
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Citation
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.378, no.4, pp.783 - 788
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.
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DOI
http://dx.doi.org/10.1016/j.bbrc.2008.11.122
ISSN
0006-291X
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