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

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Lysophosphatidylcholine Activates Adipocyte Glucose Uptake and Lowers Blood Glucose Levels in Murine Models of Diabetes

Cited 22 times inthomson ciCited 20 times inthomson ci
Title
Lysophosphatidylcholine Activates Adipocyte Glucose Uptake and Lowers Blood Glucose Levels in Murine Models of Diabetes
Author
Yea, KyungmooKim, JaeyoonYoon, Jong HyukKwon, TaewanKim, Jong HyunLee, Byoung DaeLee, Hae-JeongLee, Seung JaeKim, Jong-InLee, Taehoon G.Baek, Moon-ChangPark, Ho SeonPark, Kyong SooOhba, MotoiSuh, Pann-GhillRyu, Sung Ho
Keywords
3T3-L1 adipocytes; Acyl chain; Adipocytes; Blood glucose level; Cellular function; Dominant negative; Glucose homeostasis; Glucose level; Glucose production; Glucose uptake; In-line; Kinase inhibitors; LY294002; Lysophosphatidylcholine; Mode of action; Mouse models; Murine model; Plasma membranes; Polar headgroups; Pre-Treatment; Protein Kinase C
Issue Date
200912
Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
Citation
JOURNAL OF BIOLOGICAL CHEMISTRY, v.284, no.49, pp.33833 - 33840
Abstract
Glucose homeostasis is maintained by the orchestration of peripheral glucose utilization and hepatic glucose production, mainly by insulin. In this study, we found by utilizing a combined parallel chromatography mass profiling approach that lysophosphatidylcholine (LPC) regulates glucose levels. LPC was found to stimulate glucose uptake in 3T3-L1 adipocytes dose- and time-dependently, and this activity was found to be sensitive to variations in acyl chain lengths and to polar head group types in LPC. Treatment with LPC resulted in a significant increase in the level of GLUT4 at the plasma membranes of 3T3-L1 adipocytes. Moreover, LPC did not affect IRS-1 and AKT2 phosphorylations, and LPC-induced glucose uptake was not influenced by pretreatment with the PI 3-kinase inhibitor LY294002. However, glucose uptake stimulation by LPC was abrogated both by rottlerin (a protein kinase Cδ inhibitor) and by the adenoviral expression of dominant negative protein kinase Cδ. In line with its determined cellular functions, LPC was found to lower blood glucose levels in normal mice. Furthermore, LPC improved blood glucose levels in mouse models of type 1 and 2 diabetes. These results suggest that an understanding of the mode of action of LPC may provide a new perspective of glucose homeostasis.
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DOI
http://dx.doi.org/10.1074/jbc.M109.024869
ISSN
0021-9258
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