Glucose oxidation to carboxylic products with chemocatalysts

2020 ◽  
pp. 33-60
Author(s):  
Nidhi Aggarwal ◽  
Muhamad Aadil Yatoo ◽  
Shunmugavel Saravanamurugan
Keyword(s):  
Glucose Oxidation

Amino acid-induced impairment of glucose oxidation by isolated rat muscle: mechanism of action

2007 ◽  
Vol 115 (S 1) ◽  
Author(s):  
K Stadlbauer ◽  
B Brunmair ◽  
Z Szöcs ◽  
M Krebs ◽  
A Luger ◽  
...  
Keyword(s):  
Amino Acid ◽  
Mechanism Of Action ◽  
Glucose Oxidation ◽  
Rat Muscle ◽  
Isolated Rat

scholarly journals Effects of peroral alanine administration in lactating ewes with decreased availability of glucose

1997 ◽  
Vol 78 (5) ◽  
pp. 805-813 ◽  
Author(s):  
Kjell Holtenius ◽  
Paul Holtenius
Keyword(s):  
Fatty Acids ◽  
Plasma Level ◽  
Free Fatty Acids ◽  
Skeletal Muscles ◽  
Plasma Insulin ◽  
Glucose Oxidation ◽  
Negative Energy ◽  
Crossover Design ◽  
Metabolic Effects ◽  
Significant Elevation

The metabolic effects of a phlorizin-induced drainage of glucose were studied in six lactating ewes with or without peroral alanine drenches in a study of crossover design. Phlorizin gave rise to a small, but significant, elevation of plasma β-hydroxybutyrate. The plasma level of alanine decreased by about 30 % due to the phlorizin injections and alanine was negatively correlated to β-hydroxybutyrate. The plasma level of free fatty acids increased due to phlorizin. Plasma insulin and glucose concentrations were not significantly affected by phlorizin while glucagon level showed a small but significant increase. Peroral alanine drenches to phlorizin-treated ewes gave rise to a transitory elevation of alanine in plasma. The plasma level of free fatty acids was about 40 % lower in phlorizin-treated ewes receiving alanine and β-hydroxybutyrate tended to be lower (P < 0.08). We suggest that β-hydroxybutyrate, apart from its function as an oxidative fuel, might play an important role by limiting glucose oxidation and protein degradation in skeletal muscles during periods of negative energy balance in ruminants. Furthermore, it is suggested that alanine supplementation decreases lipolysis and ketogenesis in lactating ewes.

Metabolic and endothelial effects of trimetazidine on forearm skeletal muscle in patients with type 2 diabetes and ischemic cardiomyopathy

2006 ◽  
Vol 290 (1) ◽  
pp. E54-E59 ◽  
Author(s):  
Lucilla D. Monti ◽  
Emanuela Setola ◽  
Gabriele Fragasso ◽  
Riccardo P. Camisasca ◽  
Pietro Lucotti ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Lipid Oxidation ◽  
Ischemic Cardiomyopathy ◽  
Glucose Oxidation ◽  
Diabetic Patients ◽  
Vascular Effects ◽  
Type 2 Diabetic Patients ◽  
Double Blind ◽  
Endothelin 1

The aim of the present study was to evaluate the effect of prolonged inhibition of β-oxidation on glucose and lipid muscle forearm metabolism and cGMP and endothelin-1 forearm release in patients with type 2 diabetes mellitus and ischemic cardiomyopathy. Fifteen patients were randomly allocated in a double-blind cross-over parallel study with trimetazidine (20 mg tid) or placebo lasting 15 days. At the end of each period, all patients underwent euglycemic hyperinsulinemic clamps with forearm indirect calorimetry and endothelial balance of vasodilator and vasoconstricor factors. Compared with placebo, trimetazidine induced 1) an increase in insulin-induced forearm glucose uptake and glucose oxidation accompained by a reduction in forearm lipid oxidation and citrate release and 2) a decrease of endothelin-1 release paralleled by a significant increase in forearm cGMP release. Forearm glucose oxidation significantly correlated with cGMP release ( r = 0.37, P < 0.04), whereas forearm lipid oxidation positively correlated with endothelin-1 release ( r = 0.40, P < 0.03). In conclusion, for the first time, we demonstrated that insulin-induced forearm glucose oxidation and forearm cGMP release were increased whereas forearm endothelin-1 release was decreased during trimetazidine treatment. Muscle's metabolic and vascular effects of trimetazidine add new interest in the use of trimetazidine in type 2 diabetic patients with cardiovascular disease.

Self-Assembled Copper Nanoclusters for Electrocatalytic Glucose Oxidation

2021 ◽  
Author(s):  
Ailing Han ◽  
Yayu Yang ◽  
Xia Li ◽  
Sijia Hao ◽  
Guozhen Fang ◽  
...  
Keyword(s):  
Glucose Oxidation ◽  
Copper Nanoclusters ◽  
Self Assembled

scholarly journals N, S and Transition-Metal Co-Doped Graphene Nanocomposites as High-Performance Catalyst for Glucose Oxidation in a Direct Glucose Alkaline Fuel Cell

Nanomaterials ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 202
Author(s):  
Yexin Dai ◽  
Jie Ding ◽  
Jingyu Li ◽  
Yang Li ◽  
Yanping Zong ◽  
...  
Keyword(s):  
Fuel Cell ◽  
Active Sites ◽  
High Performance ◽  
Glucose Oxidation ◽  
Alkaline Fuel Cell ◽  
Blank Group ◽  
Graphene Nanocomposites ◽  
Doped Graphene ◽  
One Step ◽  
Hydrothermal Approach

In this work, reduced graphene oxide (rGO) nanocomposites doped with nitrogen (N), sulfur (S) and transitional metal (Ni, Co, Fe) were synthesized by using a simple one-step in-situ hydrothermal approach. Electrochemical characterization showed that rGO-NS-Ni was the most prominent catalyst for glucose oxidation. The current density of the direct glucose alkaline fuel cell (DGAFC) with rGO-NS-Ni as the anode catalyst reached 148.0 mA/cm2, which was 40.82% higher than the blank group. The DGAFC exhibited a maximum power density of 48 W/m2, which was more than 2.08 folds than that of blank group. The catalyst was further characterized by SEM, XPS and Raman. It was speculated that the boosted performance was due to the synergistic effect of N, S-doped rGO and the metallic redox couples, (Ni2+/Ni3+, Co2+/Co3+ and Fe2+/Fe3+), which created more active sites and accelerated electron transfer. This research can provide insights for the development of environmental benign catalysts and promote the application of the DGAFCs.

scholarly journals Brain energy metabolism in intracerebroventricularly administered streptozotocin mouse model of Alzheimer’s disease: A 1H-[13C]-NMR study

2021 ◽  
pp. 0271678X2199617
Author(s):  
Narayan D Soni ◽  
Akila Ramesh ◽  
Dipak Roy ◽  
Anant B Patel
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Glucose Oxidation ◽  
Neurodegenerative Disorder ◽  
Nmr Spectrum ◽  
Tissue Extracts ◽  
Model Of Alzheimer’S Disease ◽  
Nmr Study ◽  
Synaptic Neurotransmission ◽  
C Nmr

Alzheimer’s disease (AD) is a very common neurodegenerative disorder. Although a majority of the AD cases are sporadic, most of the studies are conducted using transgenic models. Intracerebroventricular (ICV) administered streptozotocin (STZ) animals have been used to explore mechanisms in sporadic AD. In this study, we have investigated memory and neurometabolism of ICV-STZ-administered C57BL6/J mice. The neuronal and astroglial metabolic activity was measured in 1H-[13C]-NMR spectrum of cortical and hippocampal tissue extracts of mice infused with [1,6-13C2]glucose and [2-13C]acetate, respectively. STZ-administered mice exhibited reduced (p = 0.00002) recognition index for memory. The levels of creatine, GABA, glutamate and NAA were reduced (p ≤ 0.04), while that of myo-inositol was increased (p < 0.05) in STZ-treated mice. There was a significant (p ≤ 0.014) reduction in aspartate-C3, glutamate-C4/C3, GABA-C2 and glutamine-C4 labeling from [1,6-13C2]glucose. This resulted in decreased rate of glucose oxidation in the cerebral cortex (0.64 ± 0.05 vs. 0.77 ± 0.05 µmol/g/min, p = 0.0008) and hippocampus (0.60 ± 0.04 vs. 0.73 ± 0.07 µmol/g/min, p = 0.001) of STZ-treated mice, due to similar reductions of glucose oxidation in glutamatergic and GABAergic neurons. Additionally, reduced glutamine-C4 labeling points towards compromised synaptic neurotransmission in STZ-treated mice. These data suggest that the ICV-STZ model exhibits neurometabolic deficits typically observed in AD, and its utility in understanding the mechanism of sporadic AD.

Effect of Thioctic Acid on Glucose Oxidation by Liver Slices

Nature ◽  
1955 ◽  
Vol 176 (4486) ◽  
pp. 788-789 ◽  
Author(s):  
J. BORNSTEIN ◽  
BERYL D. HARTMAN
Keyword(s):  
Glucose Oxidation ◽  
Thioctic Acid ◽  
Liver Slices
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