2014
DOI: 10.1152/ajpendo.00655.2013
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Calcium signaling recruits substrate transporters GLUT4 and CD36 to the sarcolemma without increasing cardiac substrate uptake

Abstract: Luiken JJ. Calcium signaling recruits substrate transporters GLUT4 and CD36 to the sarcolemma without increasing cardiac substrate uptake.

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Cited by 24 publications
(29 citation statements)
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“…6) . This dual effect would serve to adjust the capacity for FA oxidation to match FA availability and explains earlier observations in cardiomyocytes where both sarcolemmal CD36 recruitment and AMPK activation were shown important for FA oxidation [77, 78]. Furthermore, dysregulation of AMPK signaling [79] or CD36 deletion [38, 47] associates with metabolic inflexibility evidenced by a diminished capacity to adjust FA oxidation to FA availability.…”
Section: Sarcolemmal Cd36 Targets Fas To Metabolic Sitesmentioning
confidence: 57%
“…6) . This dual effect would serve to adjust the capacity for FA oxidation to match FA availability and explains earlier observations in cardiomyocytes where both sarcolemmal CD36 recruitment and AMPK activation were shown important for FA oxidation [77, 78]. Furthermore, dysregulation of AMPK signaling [79] or CD36 deletion [38, 47] associates with metabolic inflexibility evidenced by a diminished capacity to adjust FA oxidation to FA availability.…”
Section: Sarcolemmal Cd36 Targets Fas To Metabolic Sitesmentioning
confidence: 57%
“…Pharmacological stimulation of extracellular Ca 2+ entry with ionophores is sufficient to increase GLUT4 translocation in some experimental systems, such as primary cardiomyocytes (Angin et al . ). Furthermore, Ca 2+ entry is likely to be required for insulin‐stimulated glucose transport in mouse skeletal muscle (Lanner et al .…”
Section: Introductionmentioning
confidence: 97%
“…Additionally, cardio-specific LKB1-KO mice indicate a major role of LKB1 in AMPK activation in response to ischemia [15]. In cardiomyocytes from LKB1-KO mice, glucose uptake stimulation by a contraction mimetic was entirely abolished [13], whereas in rat cardiomyocytes, pharmacological inhibition of CaMKKb by the potent CaMKK inhibitor STO-609, had no effect [16]. Thus, in this experimental setting, LKB1 but not CaMKKb is required for contraction-induced glucose uptake via AMPK activation.…”
Section: Factors Upstream Of Ampk Impacting Contractioninduced Glut4 mentioning
confidence: 99%
“…CaMKKb is an alternative upstream kinase of AMPK. Upon contraction, CaMKKb is likely involved in AMPK activation in skeletal muscle [62], but not in heart [16]. Death-associated protein kinase (DAPK):: mainly known as tumor suppressor gene, whose expression is greatly reduced in various human malignancies.…”
Section: Importance Of Glut4 Translocation In Cardiac Contraction-indmentioning
confidence: 99%
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