scholarly journals Immunofluorescence microscopy of SNAP23 in human skeletal muscle reveals colocalization with plasma membrane, lipid droplets, and mitochondria

2016 ◽  
Vol 4 (1) ◽  
pp. e12662 ◽  
Author(s):  
Juliette A. Strauss ◽  
Christopher S. Shaw ◽  
Helen Bradley ◽  
Oliver J. Wilson ◽  
Thierry Dorval ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Plasma Membrane ◽  
Lipid Droplets ◽  
Human Skeletal Muscle ◽  
Immunofluorescence Microscopy ◽  
Membrane Lipid ◽  
Plasma Membrane Lipid

scholarly journals Membrane lipid rafts are disturbed in the response of rat skeletal muscle to short-term disuse

2017 ◽  
Vol 312 (5) ◽  
pp. C627-C637 ◽  
Author(s):  
Alexey M. Petrov ◽  
Violetta V. Kravtsova ◽  
Vladimir V. Matchkov ◽  
Alexander N. Vasiliev ◽  
Andrey L. Zefirov ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Plasma Membrane ◽  
Lipid Rafts ◽  
Lipid Raft ◽  
Motor Nerve ◽  
Membrane Lipid ◽  
Hindlimb Suspension ◽  
Cholera Toxin B Subunit ◽  
Plasma Membrane Lipid ◽  
Intracellular Ca

Marked loss of skeletal muscle mass occurs under various conditions of disuse, but the molecular and cellular mechanisms leading to atrophy are not completely understood. We investigate early molecular events that might play a role in skeletal muscle remodeling during mechanical unloading (disuse). The effects of acute (6–12 h) hindlimb suspension on the soleus muscles from adult rats were examined. The integrity of plasma membrane lipid rafts was tested utilizing cholera toxin B subunit or fluorescent sterols. In addition, resting intracellular Ca2+ level was analyzed. Acute disuse disturbed the plasma membrane lipid-ordered phase throughout the sarcolemma and was more pronounced in junctional membrane regions. Ouabain (1 µM), which specifically inhibits the Na-K-ATPase α2 isozyme in rodent skeletal muscles, produced similar lipid raft changes in control muscles but was ineffective in suspended muscles, which showed an initial loss of α2 Na-K-ATPase activity. Lipid rafts were able to recover with cholesterol supplementation, suggesting that disturbance results from cholesterol loss. Repetitive nerve stimulation also restores lipid rafts, specifically in the junctional sarcolemma region. Disuse locally lowered the resting intracellular Ca2+ concentration only near the neuromuscular junction of muscle fibers. Our results provide evidence to suggest that the ordering of lipid rafts strongly depends on motor nerve input and may involve interactions with the α2 Na-K-ATPase. Lipid raft disturbance, accompanied by intracellular Ca2+ dysregulation, is among the earliest remodeling events induced by skeletal muscle disuse.

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

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.

scholarly journals Dietary α-linolenic acid supplementation alters skeletal muscle plasma membrane lipid composition, sarcolemmal FAT/CD36 abundance, and palmitate transport rates

2016 ◽  
Vol 311 (6) ◽  
pp. R1234-R1242 ◽  
Author(s):  
Zane Chorner ◽  
Pierre-Andre Barbeau ◽  
Laura Castellani ◽  
David C. Wright ◽  
Adrian Chabowski ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acids ◽  
Plasma Membrane ◽  
Fatty Acid ◽  
Polyunsaturated Fatty Acids ◽  
Linolenic Acid ◽  
Lipid Composition ◽  
Membrane Lipid ◽  
Membrane Lipid Composition ◽  
Plasma Membrane Lipid

The cellular processes influenced by consuming polyunsaturated fatty acids remains poorly defined. Within skeletal muscle, a rate-limiting step in fatty acid oxidation is the movement of lipids across the sarcolemmal membrane, and therefore, we aimed to determine the effects of consuming flaxseed oil high in α-linolenic acid (ALA), on plasma membrane lipid composition and the capacity to transport palmitate. Rats fed a diet supplemented with ALA (10%) displayed marked increases in omega-3 polyunsaturated fatty acids (PUFAs) within whole muscle and sarcolemmal membranes (approximately five-fold), at the apparent expense of arachidonic acid (−50%). These changes coincided with increased sarcolemmal palmitate transport rates (+20%), plasma membrane fatty acid translocase (FAT/CD36; +20%) abundance, skeletal muscle triacylglycerol content (approximately twofold), and rates of whole body fat oxidation (~50%). The redistribution of FAT/CD36 to the plasma membrane could not be explained by increased phosphorylation of signaling pathways implicated in regulating FAT/CD36 trafficking events (i.e., phosphorylation of ERK1/2, CaMKII, AMPK, and Akt), suggesting the increased n-3 PUFA composition of the plasma membrane influenced FAT/CD36 accumulation. Altogether, the present data provide evidence that a diet supplemented with ALA increases the transport of lipids into resting skeletal muscle in conjunction with increased sarcolemmal n-3 PUFA and FAT/CD36 contents.

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

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
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