scholarly journals Inhibition of sphingomyelin synthase (SMS) affects intracellular sphingomyelin accumulation and plasma membrane lipid organization

2007 ◽  
Vol 1771 (9) ◽  
pp. 1186-1194 ◽  
Author(s):  
Zhiqiang Li ◽  
Tiruneh K. Hailemariam ◽  
Hongwen Zhou ◽  
Yan Li ◽  
Dale C. Duckworth ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Membrane Lipid ◽  
Sphingomyelin Synthase ◽  
Plasma Membrane Lipid ◽  
Lipid Organization

Alterations in plasma membrane lipid organization during lymphocyte differentiation

1986 ◽  
Vol 126 (3) ◽  
pp. 379-388 ◽  
Author(s):  
Brian J. Del Buono ◽  
Patrick L. Williamson ◽  
Robert A. Schlegel
Keyword(s):  
Plasma Membrane ◽  
Membrane Lipid ◽  
Lymphocyte Differentiation ◽  
Plasma Membrane Lipid ◽  
Lipid Organization

scholarly journals Lysophospholipid acylation modulates plasma membrane lipid organization and insulin sensitivity in skeletal muscle

2021 ◽  
Vol 131 (8) ◽  
Author(s):  
Patrick J. Ferrara ◽  
Xin Rong ◽  
J. Alan Maschek ◽  
Anthony R.P. Verkerke ◽  
Piyarat Siripoksup ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Plasma Membrane ◽  
Insulin Sensitivity ◽  
Membrane Lipid ◽  
Plasma Membrane Lipid ◽  
Lipid Organization

Plasma membrane lipid organization and the adherence of differentiating lymphocytes to macrophages

1989 ◽  
Vol 138 (1) ◽  
pp. 61-69 ◽  
Author(s):  
Brian J. Del Buono ◽  
Scott M. White ◽  
Patrick L. Williamson ◽  
Robert A. Schlegel
Keyword(s):  
Plasma Membrane ◽  
Membrane Lipid ◽  
Plasma Membrane Lipid ◽  
Lipid Organization

scholarly journals The Lands cycle modulates plasma membrane lipid organization and insulin sensitivity in skeletal muscle

2019 ◽  
Author(s):  
Patrick J. Ferrara ◽  
Xin Rong ◽  
J. Alan Maschek ◽  
Anthony R.P. Verkerke ◽  
Piyarat Siripoksup ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Plasma Membrane ◽  
Insulin Sensitivity ◽  
Ex Vivo ◽  
Membrane Lipid ◽  
Insulin Resistant ◽  
Skeletal Muscle Insulin Resistance ◽  
Plasma Membrane Lipid ◽  
Lipid Organization

AbstractAberrant lipid metabolism promotes the development of skeletal muscle insulin resistance, but the exact identity of lipid-mediated mechanisms relevant to human obesity remains unclear. A comprehensive lipidomic analyses of primary myocytes from lean insulin-sensitive (LN) and obese insulin-resistant (OB) individuals revealed several species of lysophospholipids (lyso-PL) that were differentially-abundant. These changes coincided with greater expression of lysophosphatidylcholine acyltransferase 3 (LPCAT3), an enzyme involved in phospholipid transacylation (Lands cycle). Strikingly, mice with skeletal muscle-specific knockout of LPCAT3 (LPCAT3-MKO) exhibited greater muscle lyso-PC/PC, concomitant with greater insulin sensitivity in vivo and insulin-stimulated skeletal muscle glucose uptake ex vivo. Absence of LPCAT3 reduced phospholipid packing of the cellular membranes and increased plasma membrane lipid clustering, suggesting that LPCAT3 affects insulin receptor phosphorylation by modulating plasma membrane lipid organization. In conclusion, obesity accelerates the skeletal muscle Lands cycle, whose consequence might induce the disruption of plasma membrane organization that suppresses muscle insulin action.

Dietary fat ratios and liver plasma membrane lipid composition

Lipids ◽  
1988 ◽  
Vol 23 (9) ◽  
pp. 829-833 ◽  
Author(s):  
Michael W. Hamm ◽  
Anna Sekowski ◽  
Roni Ephrat
Keyword(s):  
Plasma Membrane ◽  
Lipid Composition ◽  
Dietary Fat ◽  
Membrane Lipid ◽  
Membrane Lipid Composition ◽  
Liver Plasma Membrane ◽  
Plasma Membrane Lipid

1P-0227 Apolipoprotein A-1 interaction with plasma membrane lipid rafts controls cholesterol export from macrophages

2003 ◽  
Vol 4 (2) ◽  
pp. 69 ◽  
Author(s):  
W. Jessup ◽  
K. Gaus ◽  
L. Kritharides ◽  
A. Boettcher ◽  
W. Drobnik ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Lipid Rafts ◽  
Membrane Lipid ◽  
Apolipoprotein A ◽  
Plasma Membrane Lipid

Time-Course of Changes in the Plasma–Membrane Lipid Bilayer and Cellular Ultrastructure Induced by Tumour Necrosis Factor-α in K 562 and Daudi Cells

1995 ◽  
Vol 23 (4) ◽  
pp. 254-263 ◽  
Author(s):  
M Marutaka ◽  
H Iwagaki ◽  
K Mizukawa ◽  
N Tanaka ◽  
K Orita
Keyword(s):  
Plasma Membrane ◽  
Cell Membrane ◽  
Membrane Fluidity ◽  
Time Course ◽  
Membrane Lipid ◽  
Plasma Membrane Lipid ◽  
Membrane Lipid Bilayer ◽  
Cell Membrane Fluidity ◽  
K 562 Cells ◽  
Factor Α

The time-course of changes in the plasma-membrane lipid bilayer induced by tumour necrosis factor-α (TNF) were investigated in cultured cells using spin-label electron-spin-resonance techniques. Treatment of K 562 cells, a human chronic myelocytic leukaemia cell line, in suspension culture with TNF for up to 6 h caused an initial increase in cell-membrane fluidity, which returned to the control level after 12 h of treatment. After 24 h of treatment, the cell-membrane fluidity had decreased and this decrease was maintained after 48 h of treatment. In Daudi cells, a human malignant lymphoma cell line, TNF, did not induce any changes in cell-membrane fluidity, indicating that the effect of TNF on membrane structure is cell-specific. The early and transient change in membrane fluidity in K 562 cells is probably related to signal generation, while the later, persistent change may reflect the phenotype of TNF-treated cells, in particular, changes in the plasma membrane-cytoplasmic complex. Histochemical electron microscopic studies indicated that the membrane fluidity changes induced by TNF have an ultrastructural correlate.

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