Inhibitory Effect of Fatty Acids on Glucose and Insulin Uptake in the Perfused Rat Hindquarter

Ikeda, Tadasu; Terasawa, Hikari; Ishimura, Masahiko; Ochi, Hiroshi; Noguchi, Isamu; Fujiyama, K.; Hoshino, Tazue; Tanaka, Yasushi; Mashiba, Hiroto

doi:10.1006/bmmb.1994.1039

Cited by 2 publications

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“…This delay may be necessary for the formation of critical levels of IMCL and lipid intermediates such as long chain fatty acyl‐coenzyme A (LCFACoA), diacylglycerol (DAG) or ceramide [5], compounds which have independently been shown to disturb normal insulin signalling in myocytes [8,20–22]. However, when compared with those normally observed after glucose‐stimulated hyperinsulinaemia, the supraphysiological plasma insulin concentrations (∼400 pmol/l) employed in these studies [4–9] may have confounded measurement of the effect of hyperlipidaemia on insulin‐mediated glucose uptake [23,24]. Thus, a possible independent effect of FFAs on the insulin/glucose interaction under physiological conditions cannot be excluded.…”

Section: Introductionmentioning

confidence: 99%

Short‐term suppression of plasma free fatty acids fails to improve insulin sensitivity when intramyocellular lipid is elevated

et al. 2006

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Section: Introductionmentioning

confidence: 99%

Short‐term suppression of plasma free fatty acids fails to improve insulin sensitivity when intramyocellular lipid is elevated

et al. 2006

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Fatty acids inhibit insulin-mediated glucose transport associated with actin remodeling in rat L6 muscle cells

et al. 2010

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In skeletal muscle cells, insulin stimulates cytoskeleton actin remodeling to facilitate the translocation of glucose transporter GLUT4 to plasma membrane. Defect of insulin-induced GLUT4 translocation and actin remodeling may cause insulin resistance. Free fatty acids cause insulin resistance in skeletal muscle. The aim of this study was to investigate the effects of fatty acids on glucose transport and actin remodeling. Differentiated L6 muscle cells expressing c-myc epitope-tagged GLUT4 were treated with palmitic acid, linoleic acid and oleic acid. Surface GLUT4 and 2-deoxyglucose uptake were measured in parallel with the morphological imaging of actin remodeling and GLUT4 immunoreactivity with fluorescence, confocal and transmission electron microscopy. Differentiated L6 cells showed concentration responses of insulin-induced actin remodeling and glucose uptake. The ultrastructure of insulin-induced actin remodeling was cell projections clustered with actin and GLUT4. Acute and chronic treatment with the 3 fatty acids had no effect on insulin-induced actin remodeling and GLUT4 immunoreactivity. However, insulin-mediated glucose uptake significantly decreased by palmitic acid (25, 50, 75, 100 μmol/L), oleic acid (180, 300 μmol/L) and linoleic acid (120, 180, 300 μmol/L). Oleic acid (120, 300 μmol/L) and linoleic acid (300 μmol/L), but not palmitic acid, significantly decreased insulin-mediated GLUT4 translocation. These data suggest that fatty acids inhibit insulin-induced glucose transport associated with actin remodeling in L6 muscle cells.

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Inhibitory Effect of Fatty Acids on Glucose and Insulin Uptake in the Perfused Rat Hindquarter

Cited by 2 publications

References 0 publications

Short‐term suppression of plasma free fatty acids fails to improve insulin sensitivity when intramyocellular lipid is elevated

Short‐term suppression of plasma free fatty acids fails to improve insulin sensitivity when intramyocellular lipid is elevated

Fatty acids inhibit insulin-mediated glucose transport associated with actin remodeling in rat L6 muscle cells

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