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Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada
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Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada
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Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada
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Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada
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Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada
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Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada
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Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada
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Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada
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Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada
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Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada
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Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada
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oxidation secondary to the stimulation of pyruvate dehydrogenase (PDH) activity ( Almutairi et al. 2021 ), the rate-limiting enzyme of glucose oxidation ( Patel et al. 2014 ). These actions on myocardial glucose oxidation appear to be indirectly mediated
Department of Medical Cell Biology, University of Uppsala, PO Box 571, SE-751 23 Uppsala, Sweden
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Department of Medical Cell Biology, University of Uppsala, PO Box 571, SE-751 23 Uppsala, Sweden
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Department of Medical Cell Biology, University of Uppsala, PO Box 571, SE-751 23 Uppsala, Sweden
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Department of Medical Cell Biology, University of Uppsala, PO Box 571, SE-751 23 Uppsala, Sweden
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Department of Medical Cell Biology, University of Uppsala, PO Box 571, SE-751 23 Uppsala, Sweden
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. To do this, confocal microscopy and quantitative immunohistochemistry were used in conjunction with measurements of islet net uptake of glucose and glucose oxidation. For comparison, we also examined the effects of stimulated insulin release on GLUT2
Department of Cell Physiology and Metabolism, Animal Biology and Physiology, Organic Chemistry, Faculty of Medicine, University of Geneva, 1 rue Michel-Servet, 1211 Geneva 4, Switzerland Departments of
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-secretion coupling, since glucose oxidation promotes ATP generation necessary for the triggering of exocytosis signals. Elevation of plasma insulin was reported in stem-bark-treated diabetic rats ( Dimo et al . 2007 ). Accordingly, it was of importance to
Henry Wellcome Signalling Laboratories and Department of Biochemistry, School of Medical Sciences, University Walk, University of Bristol, Bristol BS8 1TD, UK
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Henry Wellcome Signalling Laboratories and Department of Biochemistry, School of Medical Sciences, University Walk, University of Bristol, Bristol BS8 1TD, UK
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Henry Wellcome Signalling Laboratories and Department of Biochemistry, School of Medical Sciences, University Walk, University of Bristol, Bristol BS8 1TD, UK
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Henry Wellcome Signalling Laboratories and Department of Biochemistry, School of Medical Sciences, University Walk, University of Bristol, Bristol BS8 1TD, UK
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Henry Wellcome Signalling Laboratories and Department of Biochemistry, School of Medical Sciences, University Walk, University of Bristol, Bristol BS8 1TD, UK
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cellular (extractable) insulin content. [U- 14 C]Glucose oxidation Islets were preincubated for 30 min at 37 °C in KRBH supplemented with 3 mM glucose and 0.5% BSA (w/v). Triplicate groups of 100 islets were then placed
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SUMMARY
The effects of luteinizing hormone releasing hormone (LH-RH) and thyrotrophin releasing hormone (TRH) on rabbit adipose tissue were studied. LH-RH increased [14C]glucose oxidation and incorporation into fatty acids and had lipolytic activity, at the same time decreasing [14C]glucose incorporation in glyceride—glycerol fractions. TRH had no significant effect on glucose oxidation or lipolysis but decreased [14C]fatty acid synthesis and [14C]glucose incorporation into glyceride—glycerol fractions.
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with 16.7 mM glucose. Effects of rapamycin on glucose utilization and glucose oxidation Glucose utilization was greater in islets incubated with 16.7 mM glucose than that in islets incubated with 2.8 mM glucose in both control (33.0±1.8, 2.8 mM glucose
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,f ) was calculated and used to determine the fetal glucose oxidation fraction and GOR (µmol/min) with the following equations: 14 CO 2 R p,f (dpm/min) = [ f × (a − v) 14 CO 2 concentration difference (dpm/mL)]; glucose oxidation fraction
Institute for Health and Sport (iHeS), Victoria University, Melbourne, Victoria, Australia
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Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia
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in a number of metabolic alterations. These included increased whole-body glucose oxidation, altered transcriptional responses to fasting and refeeding and evidence of reduced capacity for gluconeogenesis. Furthermore, the expression of hepatic DN PKD
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systematically compared our own list of differentially expressed genes with a database of lists of differentially expressed genes that were derived from the published microarray data, and identified common expression patterns. Glucose oxidation Glucose oxidation
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David Geffen School of Medicine, University of California-Los Angeles, Los Angeles, California, USA
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VA San Diego Healthcare System, San Diego, California, USA
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VA San Diego Healthcare System, San Diego, California, USA
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VA San Diego Healthcare System, San Diego, California, USA
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running speed and endurance in the treadmill exercise in Chga -KO mice are due to the decrease in glucose uptake and glycolysis and defects in glucose oxidation caused by defective mitochondria. In addition, the lack of adaptation to endurance exercise