scholarly journals Kinetics of L-Theanine Uptake and Metabolism in Healthy Participants Are Comparable after Ingestion of L-Theanine via Capsules and Green Tea

2012 ◽  
Vol 142 (12) ◽  
pp. 2091-2096 ◽  
Author(s):  
Lisa Scheid ◽  
Sabine Ellinger ◽  
Birgit Alteheld ◽  
Hannes Herholz ◽  
Jörg Ellinger ◽  
...  
1997 ◽  
Vol 49 (2) ◽  
pp. 157-163 ◽  
Author(s):  
Muriel Raveton ◽  
Patrick Ravanel ◽  
Anne Marie Serre ◽  
Françoise Nurit ◽  
Michel Tissut

2018 ◽  
Vol 106 ◽  
pp. 149-155 ◽  
Author(s):  
Rijuta Ganesh Saratale ◽  
Hee-Seok Lee ◽  
Yong Eui Koo ◽  
Ganesh Dattatraya Saratale ◽  
Young Jun Kim ◽  
...  

1983 ◽  
Vol 210 (1) ◽  
pp. 157-166 ◽  
Author(s):  
C A Watkins ◽  
S A Wartell ◽  
D E Rannels

The effect of halothane (2-bromo-2-chloro-1,1,1-trifluoroethane) on the uptake of 14C-labelled 5-hydroxytryptamine (5-HT) and its metabolism to 5-hydroxyindol-3-ylacetic acid (5-HIAA) was investigated in rat lungs perfused in situ. The rate of accumulation of 14C-labelled 5-HIAA in the tissue, monitored as an index of 5-HT metabolism, was linear with time, displayed saturation kinetics and remained stable for at least 180 min of perfusion. Exposure of the lungs to halothane (4%) for 60 min reversibly reduced production of 5-HIAA through an increase in the apparent Km for metabolism of the amine from 1.45 to 3.52 microM (P less than 0.001); the anaesthetic had no effect on the Vmax. of the process. The magnitude of the inhibition increased with time of exposure to the anaesthetic. Halothane exposure did not alter the distribution of [3H]sorbitol or [14C]5-HT, pulmonary vascular resistance, levels of ATP or the kinetics of amino acid transport in the tissue. Inhibition of protein synthesis by cycloheximide did not mimic the effect of the anaesthetic. These observations, together with those made in lungs exposed to inhibitors of 5-HT uptake and metabolism, were consistent with a halothane-mediated inhibition of 5-HT uptake, which did not appear to involve non-specific changes in membrane permeability.


1992 ◽  
Vol 16 (1) ◽  
pp. 5-10 ◽  
Author(s):  
Anna Mae Diehl ◽  
Shi Qi Yang ◽  
Nesbitt Brown ◽  
Jeff Smith ◽  
David Raiford ◽  
...  

1987 ◽  
Vol 15 (2) ◽  
pp. 201-215 ◽  
Author(s):  
John H. Linehan ◽  
Thomas A. Bronikowski ◽  
Christopher A. Dawson

Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 1090 ◽  
Author(s):  
Edward J. Okello ◽  
Joshua Mather

Alzheimer’s disease (AD) is characterised by the apoptosis of cholinergic neurons and the consequent attenuation of acetylcholine mediated neurotransmission, resulting in neurodegeneration. Acetyl-cholinesterase (AChE) and butyryl-cholinesterase (BuChE) are attractive therapeutic targets in the treatment of AD since inhibition of these enzymes can be used to restore synaptic concentrations of acetylcholine. Whilst inhibitors for these enzymes such as galantamine and rivastigmine have been approved for use, none are able to halt the progression of AD and are responsible for the production of troublesome side-effects. Efficacious cholinesterase inhibitors have been isolated from natural plant-based compounds with many demonstrating additional benefits beyond cholinesterase inhibition, such as antioxidation and anti-inflammation, which are key parts of AD pathology. In this study, five natural flavan-3-ol (catechin) compounds: ((-)-epicatechin (EC), catechin, (-)-epicatechin-3-gallate (ECG),) (-)-epigallocatechin (EGC), (-)-epigallocatechin-3-gallate (EGCG), isolated from green tea, were screened for their cholinesterase inhibitory activity using the Ellman assay. The kinetics of inhibition was determined using reciprocal Lineweaver-Burk plots. EGCG was the only compound found to produce statistically significant, competitive inhibition, of both AChE (p < 0.01) and BuChE (p < 0.01) with IC50 values of 0.0148 µmol/mL and 0.0251 µmol/mL respectively. These results, combined with previously identified antioxidative and anti-inflammatory properties, highlight the potential use of EGCG in the treatment of AD, provided it can be delivered to cholinergic neurons in therapeutic concentrations. Further testing of EGCG in vivo is recommended to fully characterise the pharmacokinetic properties, optimal method of administration and efficacy of this novel plant-based compound.


2019 ◽  
Vol 60 (6) ◽  
pp. 1121-1135 ◽  
Author(s):  
Boluwatiwi O. Durojaye ◽  
Kenneth M. Riedl ◽  
Robert W. Curley ◽  
Earl H. Harrison

β-Apocarotenoids are eccentric cleavage products of carotenoids formed by chemical and enzymatic oxidations. They occur in foods containing carotenoids and thus might be directly absorbed from the diet. However, there is limited information about their intestinal absorption. The present research examined the kinetics of uptake and metabolism of β-apocarotenoids. Caco-2 cells were grown on 6-well plastic plates until a differentiated cell monolayer was achieved. β-Apocarotenoids were prepared in Tween 40 micelles, delivered to differentiated cells in serum-free medium, and incubated at 37°C for up to 8 h. There was rapid uptake of β-apo-8′-carotenal into cells, and β-apo-8′-carotenal was largely converted to β-apo-8′-carotenoic acid and a minor metabolite that we identified as 5,6-epoxy-β-apo-8′-carotenol. There was also rapid uptake of β-apo-10′-carotenal into cells, and β-apo-10′-carotenal was converted into a major metabolite identified as 5,6-epoxy-β-apo-10′-carotenol and a minor metabolite that is likely a dihydro-β-apo-10′-carotenol. Finally, there was rapid cellular uptake of β-apo-13-carotenone, and this compound was extensively degraded. These results suggest that dietary β-apocarotenals are extensively metabolized in intestinal cells via pathways similar to the metabolism of retinal. Thus, they are likely not absorbed directly from the diet.


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