Insulin-like action of catecholamines and Ca2+ to stimulate glucose transport and GLUT4 translocation in perfused rat heart

Rattigan, Stephen; Appleby, Geoffrey J.; Clark, Michael G.

doi:10.1016/0167-4889(91)90012-m

Cited by 59 publications

(23 citation statements)

References 31 publications

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“…Catecholamines can increase glucose uptake and the translocation of GLUT1 and GLUT4 in perfused heart, thus may play a role in mediating GLUTs translocation during exercise and ischemia (50,179). In isolated cardiomyocytes, both alpha and beta-adrenergic stimulation lead to increases in glucose uptake, independent of changes in contraction (58).…”

Section: Glucose Transporter In the Heartmentioning

confidence: 99%

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Glucose Transporters in Cardiac Metabolism and Hypertrophy

Shao

Tian

2015

Comprehensive Physiology

200

173

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The heart is adapted to utilize all classes of substrates to meet the high-energy demand, and it tightly regulates its substrate utilization in response to environmental changes. Although fatty acids are known as the predominant fuel for the adult heart at resting stage, the heart switches its substrate preference toward glucose during stress conditions such as ischemia and pathological hypertrophy. Notably, increasing evidence suggests that the loss of metabolic flexibility associated with increased reliance on glucose utilization contribute to the development of cardiac dysfunction. The changes in glucose metabolism in hypertrophied hearts include altered glucose transport and increased glycolysis. Despite the role of glucose as an energy source, changes in other nonenergy producing pathways related to glucose metabolism, such as hexosamine biosynthetic pathway and pentose phosphate pathway, are also observed in the diseased hearts. This article summarizes the current knowledge regarding the regulation of glucose transporter expression and translocation in the heart during physiological and pathological conditions. It also discusses the signaling mechanisms governing glucose uptake in cardiomyocytes, as well as the changes of cardiac glucose metabolism under disease conditions.

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Section: Glucose Transporter In the Heartmentioning

confidence: 99%

“…In contracting hearts, increasing workload is associated with increased glucose transporter translocation and enhanced glucose uptake (179,253). Since calcium is an essential player for mediating cardiomyocyte contraction, it is reasoned that calcium may mediate glucose transport in cardiomyocytes.…”

Section: Glucose Transporter In the Heartmentioning

confidence: 99%

Glucose Transporters in Cardiac Metabolism and Hypertrophy

Shao

Tian

2015

Comprehensive Physiology

200

173

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“…In this study, we have found that failure of insulin-mediated recruitment of GLUT-4 to the plasma membrane is responsible for impaired glucose transport in hypertrophied myocardium. Besides insulin, stimuli such as exercise, hypoxia, hormones, and ischemia have also been shown to cause translocation of GLUT-4 molecules in fat and skeletal muscle [16,31,[35][36][37][38]. Diabetic myocardium and potentially other states of insulin-resistance appear to have an impaired ability to increase glucose uptake in response to either insulin or ischemia [39][40][41][42].…”

mentioning

confidence: 99%

Impaired insulin-signaling in hypertrophied hearts contributes to ischemic injury

Friehs

Cao-Danh

Nathan

et al. 2005

Biochemical and Biophysical Research Communications

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Despite increased glucose utilization by hypertrophied myocardium, these hearts exhibit a slower rate of glucose uptake (GU). We hypothesized that, in hypertrophied myocardium, a defect of the insulin-responsive glucose transporter is responsible for impaired GU and metabolism during ischemia, contributing to post-ischemic myocardial dysfunction. In a rabbit model of pressure-overload hypertrophy, GU ((31)P NMR spectroscopy) and total/phosphorylated insulin-signaling intermediates were assayed: insulin-receptor, insulin-receptor-substrate-1 (IRS-1), phosphatidylinositol-3-kinase (PI3-k), GLUT-4 translocation and contractile function in an isolated heart ischemia/reperfusion model. Total protein was not different between hypertrophied and control hearts. Phosphorylation of IRS-1 and PI3-k activity was significantly lower in hypertrophy during ischemia. GU was impaired pre-ischemia in hypertrophy, remained lower during early reperfusion, and was associated with impaired recovery of contractile function. In conclusion, a defect in IRS-1 phosphorylation and PI3-k activation in hypertrophied hearts restricts insulin-mediated GLUT-4 translocation and ischemia, a known stimulus of GLUT-4 translocation, does not compensate for this defect.

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“…Few data exist regarding the influence of PTH on carbohydrate metabolism and no previous studies have investigated the role of PTH in modulating glucose transport processes. However, in other mesenchymal cell types, agents such as forskolin and isoproterenol that increase intracellular cAMP levels have potent modulating effects on insulinstimulated glucose transport and insulin receptor tyrosine kinase activity (Lonnroth et al 1987, Tanti et al 1987, James et al 1989, Rattigan et al 1991). …”

Section: Introductionmentioning

confidence: 98%

Modulation of glucose transport by parathyroid hormone and insulin in UMR 106–01, a clonal rat osteogenic sarcoma cell line

Thomas¹,

Rogers²,

Sleeman³

et al. 1995

Journal of Molecular Endocrinology

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This study characterizes the actions of insulin and parathyroid hormone (PTH) on the glucose transport system in the rat osteogenic sarcoma cell line UMR 106-01, which expresses a number of features of the osteoblast phenotype. Using [1,2-3H]2-deoxyglucose (2-DOG) as a label, UMR 106-01 cells were shown to possess a glucose transport system which was enhanced by insulin. In contrast, PTH influenced glucose transport in a biphasic manner with a stimulatory effect at 1 h and a more potent inhibitory effect at 16 h on basal and insulin-stimulated 2-DOG transport. To explore the mechanism of PTH action, a direct agonist of cAMP-dependent protein kinase (PKA) was tested. 8-Bromo-cAMP had no acute stimulatory effect but inhibited basal and insulin-stimulated 2-DOG transport at 16 h. This result suggested that the prolonged, but not the acute, effect of PTH was mediated by the generation of cAMP. Further studies with the cell line UMR 4-7, a UMR 106-01 clone stably transfected with an inducible mutant inactive regulatory subunit of PKA, confirmed that the inhibitory but not the stimulatory effect of PTH was mediated by the PKA pathway. Northern blot data indicated that the prolonged inhibitory effects of PTH and 8-bromo-cAMP on glucose transport were likely to be mediated in part by reduction in the levels of GLUT1 (HepG2/brain glucose transporter) mRNA.

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Insulin-like action of catecholamines and Ca2+ to stimulate glucose transport and GLUT4 translocation in perfused rat heart

Cited by 59 publications

References 31 publications

Glucose Transporters in Cardiac Metabolism and Hypertrophy

Glucose Transporters in Cardiac Metabolism and Hypertrophy

Impaired insulin-signaling in hypertrophied hearts contributes to ischemic injury

Modulation of glucose transport by parathyroid hormone and insulin in UMR 106–01, a clonal rat osteogenic sarcoma cell line

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