Insulin-Induced Glucose Transporter (GLUT1 and GLUT4) Translocation in Cardiac Muscle Tissue Is Mimicked by Bradykinin

Rett, K.; Wicklmayr, M.; Dietze, Gabriele; Häring, H.-U.

doi:10.2337/diab.45.1.s66

Cited by 82 publications

(47 citation statements)

References 15 publications

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“…5,7 However, these previous studies were performed in vitro at supraphysiological insulin concentrations. The present study expands on these previous reports by examining the effects of physiological hyperinsulinemia when the heart is exposed to other substrates and performing physiological work in vivo.…”

Section: Insulin-mediated Translocation Of Glut1 and Glut4mentioning

confidence: 99%

“…8 The present study is the first to demonstrate in vivo effects of insulin on GLUT1 translocation and is consistent with previous in vitro reports that insulin stimulates GLUT1 translocation in isolated cardiomyocytes 12 and the perfused obese Zucker rat heart. 5 There is also indirect evidence, based on immunoblot analysis of intracellular membrane proteins, that insulin causes GLUT1 translocation in vitro in the perfused normal rat heart. 13 Although insulin-mediated translocation of GLUT4 requires activation of phosphatidylinositol 3-kinase, 14 the mechanism responsible for insulinmediated GLUT1 translocation remains unknown.…”

Section: Insulin-mediated Translocation Of Glut1 and Glut4mentioning

confidence: 99%

“…The GLUT1 present in heart localizes predominantly to cardiomyocytes and also translocates to the sarcolemma in response to ischemia. 4 Although one recent in vitro study has demonstrated an insulin-mediated increase in sarcolemmal GLUT1 in cultured cardiomyocytes, 5 the effect of hyperinsulinemia on myocardial GLUT1 distribution in vivo is unknown. GLUT4 translocates from an intracellular pool to the cell surface in response to insulin in skeletal 6 and heart 7 muscle.…”

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confidence: 99%

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Additive Effects of Hyperinsulinemia and Ischemia on Myocardial GLUT1 and GLUT4 Translocation In Vivo

Russell

Yin²,

Caplan³

et al. 1998

Circulation

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Background-Myocardial ischemia increases glucose uptake through the translocation of GLUT1 and GLUT4 from an intracellular compartment to the sarcolemma. The present study was performed to determine whether hyperinsulinemia causes translocation of myocardial GLUT1 as well as GLUT4 in vivo and whether there are additive effects of insulin and ischemia on GLUT1 and GLUT4 translocation. Methods and Results-Myocardial glucose uptake and transporter distribution were assessed by arteriovenous measurements, cell fractionation, and immunofluorescence. In fasted anesthetized dogs, hyperinsulinemia increased myocardial glucose extraction 3-fold (PϽ0.01) and the sarcolemmal content of GLUT4 by 90% and GLUT1 by 50% (PϽ0.05 for both) compared with saline infusion. In subsequent experiments, glucose uptake and transporter distribution were determined in ischemic and nonischemic regions of hearts from hyperinsulinemic animals during regional myocardial ischemia. Glucose uptake was 50% greater in the ischemic region (PϽ0.05). This was associated with a 20% increase in sarcolemmal GLUT1 and a 60% increase in sarcolemmal GLUT4 contents in the ischemic region (PϽ0.05 for both). Conclusions-Insulin stimulates myocardial glucose utilization through translocation of GLUT1 as well as GLUT4.Insulin and ischemia have additive effects to increase in vivo glucose utilization and augment glucose transporter translocation. We conclude that recruitment of both GLUT1 and GLUT4 contributes to increased myocardial glucose uptake during moderate reductions in coronary blood flow under insulin-stimulated conditions. (Circulation. 1998;98:2180-2186.)

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Section: Insulin-mediated Translocation Of Glut1 and Glut4mentioning

confidence: 99%

Section: Insulin-mediated Translocation Of Glut1 and Glut4mentioning

confidence: 99%

mentioning

confidence: 99%

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Additive Effects of Hyperinsulinemia and Ischemia on Myocardial GLUT1 and GLUT4 Translocation In Vivo

Russell

Yin²,

Caplan³

et al. 1998

Circulation

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“…Insulin-stimulated GLUT-4 translocation has been widely investigated in cardiac tissue by using immunofluorescence and Western blotting (8,12,19,27). Although these studies quantify GLUT-4 translocation following insulin stimulation, they do not differentiate between the different plasma membrane types within the myocyte.…”

Section: Glut-4 Distribution and Translocationmentioning

confidence: 99%

Immunogold labeling study of the distribution of GLUT-1 and GLUT-4 in cardiac tissue following stimulation by insulin or ischemia

Davey

Garlick²,

Warley³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Whereas glucose transporter 1 (GLUT-1) is thought to be responsible for basal glucose uptake in cardiac myocytes, little is known about its relative distribution between the different plasma membranes and cell types in the heart. GLUT-4 translocates to the myocyte surface to increase glucose uptake in response to a number of stimuli. The mechanisms underlying ischemia-and insulin-mediated GLUT-4 translocation are known to be different, raising the possibility that the intracellular destinations of GLUT-4 following these stimuli also differ. Using immunogold labeling, we describe the cellular localization of these two transporters and investigate whether insulin and ischemia induce differential translocation of GLUT-4 to different cardiac membranes. Immunogold labeling of GLUT-1 and GLUT-4 was performed on left ventricular sections from isolated hearts following 30 min of either insulin, ischemia, or control perfusion. In control tissue, GLUT-1 was predominantly (76%) localized in the capillary endothelial cells, with only 24% of total cardiac GLUT-1 present in myocytes. GLUT-4 was found predominantly in myocytes, distributed between sarcolemmal and T tubule membranes (1.84 Ϯ 0.49 and 1.54 Ϯ 0.33 golds/ m, respectively) and intracellular vesicles (127 Ϯ 18 golds/ m 2 ). Insulin increased T tubule membrane GLUT-4 content (2.8 Ϯ 0.4 golds/ m, P Ͻ 0.05) but had less effect on sarcolemmal GLUT-4 (1.72 Ϯ 0.53 golds/ m). Ischemia induced greater GLUT-4 translocation to both membrane types (4.25 Ϯ 0.84 and 4.01 Ϯ 0.27 golds/ m, respectively P Ͻ 0.05). The localization of GLUT-1 suggests a significant role in transporting glucose across the capillary wall before myocyte uptake via GLUT-1 and GLUT-4. We demonstrate independent spatial translocation of GLUT-4 under insulin or ischemic stimulation and propose independent roles for T-tubular and sarcolemmal GLUT-4. glucose transporter; immunogold electron microscopy

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“…There is increasing evidence to suggest that BK enhances skeletal and cardiac muscle glycolytic flux and glucose uptake. 3,4,11 In addition, plasma BK levels have been found to be reduced in patients with diabetes. 12,13 It is clinically important to determine whether the dual inhibitory effects of OMA on BK degradation can improve whole-body and myocardial glucose metabolism, perhaps to a greater extent than ACEIs, and to study the mechanism of this putative beneficial effect.…”

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confidence: 99%

Vasopeptidase Inhibitor Omapatrilat Induces Profound Insulin Sensitization and Increases Myocardial Glucose Uptake in Zucker Fatty Rats

et al. 2003

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Background-ACE inhibitors (ACEIs) improve insulin resistance and prevent type 2 diabetes, possibly mediated by inhibition of bradykinin (BK) degradation. The vasopeptidase inhibitor omapatrilat (OMA) raises BK to a greater extent than ACEIs by dual enzyme inhibition, whereas its insulin-sensitizing effects and mechanisms have not been investigated. Methods and Results-We compared the insulin-sensitizing effects of OMA, ramipril (an ACEI), losartan (an angiotensin II type 1 receptor blocker), and placebo by 2-step euglycemic hyperinsulinemic clamp in insulin-resistant Zucker fatty rats (nϭ6 to 7 in each group). OMA resulted in a lower rate of endogenous glucose production than placebo at baseline (35Ϯ5 versus 54Ϯ4 mmol · kg Ϫ1 · min Ϫ1 , PϽ0.01), greater suppression of endogenous glucose production by low-dose insulin (73Ϯ11% versus 27Ϯ18%, PϽ0.05), and greater glucose disposal at high-dose insulin (135Ϯ5 versus 92Ϯ4 mmol · kg Ϫ1 · min

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Insulin-Induced Glucose Transporter (GLUT1 and GLUT4) Translocation in Cardiac Muscle Tissue Is Mimicked by Bradykinin

Cited by 82 publications

References 15 publications

Additive Effects of Hyperinsulinemia and Ischemia on Myocardial GLUT1 and GLUT4 Translocation In Vivo

Additive Effects of Hyperinsulinemia and Ischemia on Myocardial GLUT1 and GLUT4 Translocation In Vivo

Immunogold labeling study of the distribution of GLUT-1 and GLUT-4 in cardiac tissue following stimulation by insulin or ischemia

Vasopeptidase Inhibitor Omapatrilat Induces Profound Insulin Sensitization and Increases Myocardial Glucose Uptake in Zucker Fatty Rats

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