Transporter 43/21/2023 ![]() We reveal that phosphorylation of β2AR by GRK2 is necessary for GLUT4-mediated glucose uptake and oxidation in hearts. Breed assortiment aan Trechter, oliepeilstok voor VW Transporter IV Flatbed Vrachtwagen / Chassis (70E, 70L, 70M, 7DE, 7DL) 2.5 TDI Syncro AXL Motordelen onderdelen en andere. Further, deletion of the GRK phosphorylation site at serine 355/356 of the β2AR blocked adrenergic stimulation of glucose uptake in isolated myocytes and glucose oxidation in working hearts.Ĭonclusions: Our data define a molecular pathway that controls cardiac glucose uptake and metabolism in response to adrenergic stimulation, whereby cardiac β2AR-PI3K-Akt signaling is required for promoting GLUT4 membrane insertion, glucose uptake in myocytes, and glucose oxidation in working hearts. Activation of the cardiac β2AR promoted a Gi-PI3K-Akt cascade to increase phosphorylation of the Rab guanosine triphosphatase-activating protein TBC1D4 (also known as AS160), which promoted GLUT4 membrane insertion that increased glucose uptake in cardiomyocytes, working hearts, and in vivo. Results: Deleting the cardiac β2AR abolished adrenergic stimulation of GLUT4-mediated glucose uptake in myocytes and glucose oxidation in isolated working hearts. Isolated working hearts were used to assess glucose and oleate acid oxidation after stimulation with isoproterenol. ![]() Ventricular myocytes were isolated to examine adrenergic signaling, membrane glucose transporter 4, and glucose uptake. ![]() Methods:Transgenic mice lacking β2AR in cardiomyocytes or lacking the GRK phosphorylation of serine 355/356 of the β2AR were developed. While adrenergic stimulation increases cardiac contractility and its requirement for increased substrate metabolism to meet increased energy needs, mechanisms by which receptor controls glucose metabolism is incompletely understood. Objectives: To examine the role of adrenergic signaling in regulating glucose metabolism in the heart.īackground: Glucose is a critical fuel for cardiac function.
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