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5306. Glucose administration downregulates lipoprotein lipase activity in vivo: a study using repeated intravenous fat tolerance test

Creator:
Eliška Jindřichová, Simona Kratochvílová, and Jan Kovář
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Biochemie. Molekulární biologie. Biofyzika, experimentální medicína, lipoproteiny, glukóza, inzulin, triacylglyceroly, experimental medicine, lipoproteins, glucose, insulin, triacylglycerols, intravenous fat tolerance test, 2, and 577
Language:
English
Description:
Lipoprotein lipase (LPL) is a key factor determining the clearance of triglycerides from the circulation. The enzyme activity is tissue-specifically regulated by insulin, but it is not clear yet how insulin regulates the total LPL activity in the circulation. To answer such question, we measured LPL activity using the intravenous fat tolerance test (IVFTT) that was carried out 1 h before as well as 2 h and 4 h after oral administration of glucose (75 g) in eleven healthy male volunteers. In control experiments, no glucose was given to the subjects. Glucose administration resulted in an expected increase in plasma glucose and insulin and in a suppression of non-esterified fatty acid concentration. The LPL activity assessed in IVFTT as a k2 rate constant did not change in control experiments and decreased to 78 % and 73 % of baseline values 2 h and 4 h after glucose administration, respectively (p=0.01). Similarly, LPL activity measured in the plasma after intravenous injection of heparin at the end of the experiments was 16 % lower (p<0.05) after glucose administration. In conclusion, LPL activity is already downregulated in vivo 2 h after glucose administration. The results of our study indicate that repeated IVFTT is a promising approach for studying acute changes in LPL activity., E. Jindřichová, S. Kratochvílová, J. Kovář., and Obsahuje bibliografii a bibliografické odkazy
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

5307. Glucose as a lipolytic agent: studies on isolated rat adipocytes

Creator:
Szkudelski, T. and Szkudelska, K.
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Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, glukóza, glucose, adipocytes, 14, and 612
Language:
English
Description:
In order to elucidate the direct effect of glucose on lipolysis in isolated rat adipocytes, cells were incubated in a buffer with different concentrations of this sugar: 2, 8 or 16 mmol/l. The increase in glucose concentration from 2 mmol/l to 8 or 16 mmol/l enhanced basal lipolysis by 30% and 47 %, respectively. Epinephrine-induced lipolysis (1 m mol/l) was also increased by 31 % and 32 %, when glucose concentration was increased from 2 mmol/l to 8 or 16 mmol/l, respectively. The rise in lipolysis caused by glucose was restricted by H-89 (an inhibitor of protein kinase A, 30 µmol/l), but insulin (1 nmol/l) had no inhibitory action. The augmentation of lipolysis by glucose did not require its metabolism (as demonstrated using 2-deoxyglucose) and was due to the action of this sugar on the final steps of the lipolytic cascade, particularly on protein kinase A. However, short-term exposure of adipocytes to higher glucose concentrations did not restrict the inhibitory action of insulin on lipolysis induced by epinephrine., T. Szkudelski, K. Szkudelska., and Obsahuje bibliografii
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

5308. Glucose release as a response to glucagon in rat hepatocyte culture: involvement of NO signaling

Creator:
Hassan Farghali, Hodis, J., Nikolína Kutinová-Canová, Petr Potměšil, Eva Kmoníčková, and Zdeněk Zídek
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, farmakologie, oxid dusnatý, glukagon, jaterní buňky, pharmacology, nitric oxide, glucagon, liver cells, glycogenolysis, 14, and 612
Language:
English
Description:
Glucagon and α-adrenergic-induced glycog enolysis is realized via the agonist/adenylyl cyclase/cAMP/protein kinase signaling pathway or via the activation of phosphorylase kinase by the mobilized calcium that supports the inhibition of glycogen synthase, respectively. The role of nitric oxide (NO) in this process has not been extensively studied. The present work was directed to the question whether NO is produced during glucagon-induced glycogenolysis in rat hepatocyte in a similar way like α-adrenoceptor stimulation. Glycogen-rich hepatocyte cultures were used. NO production (NO2-) was assessed under the influence of glucagon, dibutyryl cyclic AMP (db-cAMP), forskolin, the nitric oxide synthase (NOS) inhibitors Nω-nitro-L-arginine methyl ester (L-NAME) and aminoguanidine, and the NO donor S-nitroso-N-acetyl penicillamine (SNAP). Inducible NOS (iNOS) mRNA was examined by reverse transcription-polymerase chain reaction. Glycogenolysis was followed up by estimation of medium glucose levels. The amount of glucose and NO2- released by glycogen-rich hepatocytes was increased as a result of glucagon, db-cAMP, forskolin and SNAP treatments. iNOS gene expression was upregulated by glucagon. Glycogenolysis that occurs through glucagon receptor stimulation involves NO production downstream of transduction pathways through an isoform of NO synthase. The present and previous studies document possible involvement of NO signaling in glycogenolytic response to glucagon and adrenergic agonists in hepatocytes., H. Farghali, J. Hodis, N. Kutinová-Canová, P. Potměšil, E. Kmoníčková, Z. Zídek., and Obsahuje bibliografii a bibliografické odkazy
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

5309. Glutamate Induces Different Neuronal Conditioned Responses than ACPD When Used As a Locally Ionophoresed Unconditioned Stimulus in the Cat Motor Cortex

Creator:
Woody, Ch. D.
Format:
print, bez média, and svazek
Type:
article, studie, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, fyziologie člověka, human physiology, Conditioning, Learning, Pavlov, Metabotropic receptors, Excitatory amino acids, 14, and 612
Language:
English
Description:
Single unit recordings were made from the motor cortex of conscious cats with glass micropipettes that allowed ionophoretic application of 0.5 M glutamate in 2 M NaCl or 0.5 M ACPD (1S,3R-1-amino-cyclopentane-1,3-dicarboxylic acid, a mGluR agonist) in 2 M NaCl. Activity in response to a 70 dB click (1 ms rectangular pulse to loudspeaker) was studied before, during, and immediately after applying each agent locally as a paired US (90 nA current 570 ms after click for 300 ms in combination with glabella tap). A 70 dB hiss sound was presented 4.4 sec after the click as a discriminative stimulus (DS). CS and DS were presented 10 times initially (adaptation); then CS, US plus tap, and DS (approximately 10 times as conditioning); and then CS and DS (2-10 times to test post-conditioning). Glutamate potentiated the mean, early, 8-16 ms response to the click after conditioning (t=18.2, p<0.0001), but not the baseline activity which decreased from a mean of 17 spk/sec to 7 spk/sec (t=3.71, p<0.001). Baseline activity increased to 31 spk/sec when glutamate was applied during conditioning (t=3.30, p<0.005). ACPD reduced the intermediate, 64-72 ms response to the click after conditioning (t=8.18, p<0.0001), and potentiated the late 104-112 ms response (t=15.4, p<0.0001). Baseline activity was slightly increased after conditioning with ACPD. Saline did not potentiate the response to click. The results indicate that glutamate agonists that differ in their receptor affinities can induce different CRs when used as locally applied USs to condition neuronal responses to a click CS in the motor cortex of cats., Ch. D. Woody., and Obsahuje bibliografii
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

5310. Glutathione reductase is inhibited by acetaminophen-glutathione conjugate in vitro

Creator:
Tomáš Roušar, Patrik Pařík, Otto Kučera, Bartoš, M., and Zuzana Červinková
Format:
print
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, fyziologie, physiology, acetaminophen toxicity, glutathione reductase, glutathione, hepatotoxicity, 14, and 612
Language:
English
Description:
The aim of the present work was to investigate a new mechanism likely contributing to the toxic action of acetaminophen, especially to explore the possible inhibition of glutathione reductase through an acetaminophen-glutathione conjugate (APAP-SG). APAP-SG conjugate was synthesized by organic synthesis and purified by column chromatography. The inhibitory effect of the conjugate on two types of glutathione reductase (from yeasts and rat hepatocytes) was tested spectrophotometrically. We found that the enzyme activity was reduced similarly after the treatment with 2.96 mM acetaminophenglutathione conjugate in both yeast and hepatocyte glutathione reductases (GR); the enzyme activity was inhibited to 52.7±1.5 % (2.4±0.3 mU/ml) in yeast GR (control activity was 5.6±0.3 mU/ml) and to 48.1±8.8 % (2.2±0.2 mU/ml) in rat hepatocytes lysate GR (control activity was 5.2±0.2 mU/ml). In addition, the enzyme activity (from hepatocytes lysate) was decreased to 79±7 %, 67±2 % and 39±7 %, in 0.37, 1.48 and 3.7 mM concentration of the conjugate, respectively. We found that glutathione reductase, the essential enzyme of the antioxidant system, was dose-dependently inhibited by the product of acetaminophen metabolism - the conjugate of acetaminophen and glutathione., T. Roušar ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

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