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Rastislav Dzúrik - One of the best experts on this subject based on the ideXlab platform.
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Magnesium deficiency impairs rat soleus muscle Glucose Utilization and insulin sensitivity.
Polish journal of medicine and pharmacy, 1992Co-Authors: Stefíková K, Spustová, Sebekova K, Rastislav DzúrikAbstract:Insulin resistance (IR), probably a common pathway of atherosclerosis development in various diseases, was suggested to be related to magnesium (Mg) deficiency. The in vivo observations required an in vitro extension. The study was performed on isolated rat soleus muscle incubated in Ringer bicarbonate with/without Mg. Mg deficiency inhibited basal, insulin- and tolbutamide-stimulated Glucose Utilization. Insulin-stimulated Glucose Utilization was inhibited even in the case that insulin was given to rats before sacrifice. Similar inhibition of Glucose Utilization was found in Ca deficiency and the simultaneous lack of Mg had no additive effect. It is concluded that Mg deficiency inhibits Glucose Utilization at the level of Ca mediation of Glucose transport regulation.
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Effect of Hippurate on Glucose Utilization in Rat Kidney Cortex Slices
Kidney & Blood Pressure Research, 1991Co-Authors: Viera Spustová, Rastislav DzúrikAbstract:Hippurate action on Glucose Utilization was evaluated in rat kidney cortex slices. Studies have shown the following. (1) Hippurate inhibits markedly basal as well as insulin-stimulated Glucose utiliza
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Effect of hippurate on Glucose Utilization in rat kidney cortex slices.
Renal physiology and biochemistry, 1991Co-Authors: Viera Spustová, Rastislav DzúrikAbstract:Hippurate action on Glucose Utilization was evaluated in rat kidney cortex slices. Studies have shown the following. (1) Hippurate inhibits markedly basal as well as insulin-stimulated Glucose Utilization and basal gluconeogenesis. (2) Ca deficiency and specific Ca channel blockers diltiazem and isradipine abolish the hippurate inhibition of Glucose Utilization. (3) K+ channel blockers, i.e. the increased K+ concentration in incubation medium, procaine and sulfonylurea drugs also abolish the hippurate inhibition of Glucose Utilization. It is concluded that hippurate and benzoate operate through the ATP-dependent K+ channel.
Jaseem Anwer - One of the best experts on this subject based on the ideXlab platform.
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In vivo effects of (-)-nicotine on ethanol-induced increase in Glucose Utilization in the mouse cerebellum.
Brain Research Bulletin, 1995Co-Authors: Jaseem AnwerAbstract:Abstract The purpose of this study was to investigate the possible in vivo effects of (-)-nicotine, ethanol, and an adenosine agonist N 6 -cyclohexyladenosine (CHA) when injected individually as well as in various combinations on Glucose Utilization in the fresh cerebellar slices of mice. Mice received ICV (-)-nicotine or CHA followed 5 min later by a test dose of ethanol (2 g/kg; IP). Animals were killed 20 min postethanol treatment and fresh slices (300 μm) of cerebellum were incubated in a Glucose medium in Warburg flasks using 14 C-Glucose as a tracer. Trapped 14 CO 2 was counted to estimate Glucose Utilization. Ethanol treatment markedly accentuated Glucose Utilization, whereas the pretreatment with (-)-nicotine (125 and 250 ng, ICV) resulted in a significant attenuation in the ethanol-induced increase in Glucose Utilization. However, ICV (-)-nicotine (125 ng) alone did not produce any change in the cerebellar Glucose Utilization. The attenuation of ethanol-induced increase in Glucose Utilization by (-)-nicotine was nearly totally blocked by ICV hexamethonium, a purported nicotinic antagonist, suggesting participation of cholinergic-nicotinic receptors. The (-)-nicotine pretreatment also significantly attenuated both the ICV CHA (25 ng)-induced increase in Glucose Utilization and the accentuation of ethanol-induced increase in Glucose Utilization by CHA. The antagonistic effect of (-)-nicotine on CHA- and ethanol-induced increase in Glucose Utilization indicating an interaction between (−)-nicotine and ethanol and between (-)-nicotine and adenosine may suggest involvement of postreceptor (nicotinic and adenosine) mechanisms including ionic channels.
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Possible Central Adenosinergic Modulation of Ethanol-Induced Alterations in [14C] Glucose Utilization in Mice
Alcoholism: Clinical and Experimental Research, 1995Co-Authors: Jaseem AnwerAbstract:The possible role of brain adenosine in acute ethanol-induced alteration in Glucose Utilization in the whole brain, as well as in the specific brain areas (cerebellum and brain stem), was investigated. Mice were killed 20-min postethanol, and the fresh tissue slices (300 μm) of brain and/or specific brain areas were incubated for 100 min in a 5.5 mM Glucose medium in Warburg flasks using [6- 14 C]Glucose as a tracer. Trapped 14 CO 2 was counted to estimate Glucose Utilization. Ethanol (2 g/kg, ip) markedly increased the Glucose Utilization in whole brain and in both motor areas of brain. Theophylline (50 mg/kg, ip), an adenosine antagonist, significantly reduced ethanol-induced increase in Glucose Utilization in whole brain, as well as in brain areas. However, adenosine agonist N 6 -cyclohexyladenosine (CHA ; 0.1 mg/kg, ip) on the contrary, significantly accentuated ethanol-induced increase in Glucose Utilization in these tissues that was nearly completely blocked by theophylline pretreatment Theophylline alone did not produce any significant change in Glucose Utilization, whereas CHA alone (in vivo and in vitro) significantly increased Glucose Utilization, as well as ethanol-induced increase in Glucose Utilization in an additive manner. Relevant supportive data were obtained by experiments in which adenosine deaminase (ADA), p-sulfophenyltheophylline (8-SPT), and CHA were administered in vitro to the slice preparations. Both ADA and 8-SPT were effective in almost completely blocking the ethanol-induced increase in Glucose Utilization, whereas CHA further enhanced the ethanol-induced increase in Glucose Utilization in an additive manner. Collectively, data seemed to suggest an adenosinergic modulation of ethanol-induced increase in Glucose Utilization in whole brain, as well as in the cerebellum and brain stem via specific adenosine receptors.
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Ethanol-induced alterations in sup 14 C-Glucose Utilization: Modulation by brain adenosine in mice
1992Co-Authors: Jaseem AnwerAbstract:The possible role of brain adenosine (Ado) in acute ethanol-induced alteration in Glucose Utilization in the cerebellum and brain stem was investigated. The slices were incubated for 100 min in a Glucose medium in Warburg flasks using {sup 14}C-Glucose as a tracer. Trapped {sup 14}CO{sub 2} was counted to estimate Glucose Utilization. Ethanol markedly increased the Glucose Utilization in both areas of brain. Theophylline, an Ado antagonist, significantly reduced ethanol-induced increase in Glucose Utilization in both brain areas. Ado agonist CHA significantly accentuated ethanol-induced increase in Glucose Utilization in both motor areas. Ado agonist CHA significantly accentuated ethanol-induced increase in Glucose Utilization in both motor areas. Ethanol was still able to produce a smaller but significant increase in Glucose Utilization in both brain areas when theophylline and CHA were given together, suggesting an additional mechanism. Collectively, the data indicate that ethanol-induced Glucose Utilization in the cerebellum and brain stem is modulated by brain Ado receptor and by non-adenosinergic mechanism.
Clifford S. Patlak - One of the best experts on this subject based on the ideXlab platform.
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Simplified brain slice Glucose Utilization
Journal of Cerebral Blood Flow and Metabolism, 1996Co-Authors: George C. Newman, Frank E. Hospod, Behzad Maghsoudlou, Clifford S. PatlakAbstract:Brain slice Glucose Utilization (SGU) can be measured by methods analogous to those used for in vivo cerebral Glucose Utilization. In order to make this technique more accessible and applicable to a broad range of experimental conditions, we have derived a simplified operational rate equation and generated the table of apparent rate coefficients necessary to apply the equation under different experimental situations. Calculations of the apparent rate coefficients were based upon an eight-parameter kinetic model combined with Michaelis–Menten theory to account for changes in the rate constants as a function of buffer Glucose concentration. The theory was tested with a series of experiments using rat brain slices, [14C]-2-deoxyGlucose (2DG) and [14C]-3–O-methylGlucose (3OMG). The errors involved in the simplified technique were estimated by a variety of techniques and found to be acceptable over a broad range of conditions. A detailed, practical protocol for the simplified method is presented.
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Cerebral Glucose Utilization and blood flow in adult spontaneously hypertensive rats.
Hypertension, 1992Co-Authors: Atsushi Tajima, Clifford S. Patlak, Hiroyuki Nakata, V. Acuff, Karen D. Pettigrew, Joseph D. FenstermacherAbstract:Not only blood pressure but also behavioral activity, brain morphology, and cerebral ventricular size differ between young spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. This suggests that cerebral blood flow and cerebral metabolism may vary between these two rat strains. To test this hypothesis, we measured local cerebral Glucose Utilization in 31 brain areas of 26-30-week-old rats. Local cerebral blood flow was also assessed in these same areas. Cerebral Glucose Utilization was measured by the 2-deoxyGlucose method; cerebral blood flow was determined by the iodoantipyrene method. In virtually all gray matter structures, the apparent rate of Glucose Utilization was lower in SHR than in normotensive WKY rats; the interstrain differences varied significantly among structures and were statistically significant (uncorrected t tests) in 14 of 28 gray matter areas. Local cerebral blood flow was fairly similar in the two rat strains. The coupling of blood flow to Glucose Utilization varied significantly among brain areas in normotensive WKY rats as well as in SHR. In a number of gray matter structures, the coupling of flow to metabolism differed between hypertensive and normotensive animals. These data suggest that for many brain areas, either Glucose Utilization or Glucose partitioning differs between WKY rats and SHR.
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Analysis of in vitro Glucose Utilization in a circadian pacemaker model
The Journal of Neuroscience, 1992Co-Authors: George C. Newman, Frank E. Hospod, Clifford S. Patlak, Robert Y. MooreAbstract:An in vitro Glucose Utilization method, based upon 14C-2-deoxyGlucose kinetics in brain slices, has been used to study circadian rhythms in hypothalamic slices containing the suprachiasmatic nucleus (SCN). Spontaneous SCN metabolic activity in vitro is similar to that observed in vivo with higher metabolic rates in subjective daytime and lower rates during subjective night. However, in vitro SCN metabolic activity during late subjective day is above that seen when Glucose Utilization is measured in vivo, suggesting that an inhibitory influence normally active in vivo is lost during slice isolation. Incubation of slices containing SCN in the presence of TTX exposes a TTX-insensitive component of metabolic activity in early subjective day, supporting prior suggestions that Glucose Utilization by the circadian oscillator continues in the absence of Na(+)-dependent action potentials. Studies with high Mg2+ concentrations are consistent with the hypothesis that most metabolic activity above the basal level observed with the Glucose Utilization method is related to synaptic activity. Pharmacological studies of the SCN brain slice model with radiotracers offer potential for analysis of both circadian rhythmicity and neural regulation.
George C. Newman - One of the best experts on this subject based on the ideXlab platform.
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Simplified brain slice Glucose Utilization
Journal of Cerebral Blood Flow and Metabolism, 1996Co-Authors: George C. Newman, Frank E. Hospod, Behzad Maghsoudlou, Clifford S. PatlakAbstract:Brain slice Glucose Utilization (SGU) can be measured by methods analogous to those used for in vivo cerebral Glucose Utilization. In order to make this technique more accessible and applicable to a broad range of experimental conditions, we have derived a simplified operational rate equation and generated the table of apparent rate coefficients necessary to apply the equation under different experimental situations. Calculations of the apparent rate coefficients were based upon an eight-parameter kinetic model combined with Michaelis–Menten theory to account for changes in the rate constants as a function of buffer Glucose concentration. The theory was tested with a series of experiments using rat brain slices, [14C]-2-deoxyGlucose (2DG) and [14C]-3–O-methylGlucose (3OMG). The errors involved in the simplified technique were estimated by a variety of techniques and found to be acceptable over a broad range of conditions. A detailed, practical protocol for the simplified method is presented.
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Analysis of in vitro Glucose Utilization in a circadian pacemaker model
The Journal of Neuroscience, 1992Co-Authors: George C. Newman, Frank E. Hospod, Clifford S. Patlak, Robert Y. MooreAbstract:An in vitro Glucose Utilization method, based upon 14C-2-deoxyGlucose kinetics in brain slices, has been used to study circadian rhythms in hypothalamic slices containing the suprachiasmatic nucleus (SCN). Spontaneous SCN metabolic activity in vitro is similar to that observed in vivo with higher metabolic rates in subjective daytime and lower rates during subjective night. However, in vitro SCN metabolic activity during late subjective day is above that seen when Glucose Utilization is measured in vivo, suggesting that an inhibitory influence normally active in vivo is lost during slice isolation. Incubation of slices containing SCN in the presence of TTX exposes a TTX-insensitive component of metabolic activity in early subjective day, supporting prior suggestions that Glucose Utilization by the circadian oscillator continues in the absence of Na(+)-dependent action potentials. Studies with high Mg2+ concentrations are consistent with the hypothesis that most metabolic activity above the basal level observed with the Glucose Utilization method is related to synaptic activity. Pharmacological studies of the SCN brain slice model with radiotracers offer potential for analysis of both circadian rhythmicity and neural regulation.
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Ischemic Brain Slice Glucose Utilization: Effects of Slice Thickness, Acidosis, and K+
Journal of Cerebral Blood Flow and Metabolism, 1991Co-Authors: George C. Newman, Frank E. Hospod, Scott L. SchisselAbstract:Summary: Brain slices of varying thickness were used to modify retention of metabolic products in an in vitro model of ischemia. Past and present results reveal increased anaerobic glycolysis in 660-µm slices with accumulation of lactate as slice thickness reaches 1,000 µm. Brain slice Glucose Utilization and lactate content were measured in buffers of various extracellular K+ levels and pH in 540-, 660-, and l,000-µm slices. Acidosis suppresses Glucose Utilization at all slice thicknesses without affecting tissue lactate. Studies of 2-deoxyGlucose metabolites establish that the suppression of Glucose Utilization by acidosis is due entirely to inhibition of Glucose phosphorylation without any effect on Glucose uptake into tissue. The inhibition is reversible after 45 min at pH 6.1. The experiments with acidosis also suggest that persistent energy demands continue to stimulate phosphofructoki-nase despite the low pH so that glycolysis continues, with potential for injury. Increasing K+ increases Glucose Utilization and tissue lactate at all three thicknesses. Correlations of Glucose Utilization with lactate accumulation support the possibility that high K+ may exert a dual influence on the tissue metabolism, not only stimulating Glucose Utilization by inducing depolarization but also by influencing the removal of metabolic products.
Jeremie Boucher - One of the best experts on this subject based on the ideXlab platform.
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apelin stimulates Glucose Utilization in normal and obese insulin resistant mice
Cell Metabolism, 2008Co-Authors: Cedric Dray, Claude Knauf, Daniele Daviaud, Aurelie Waget, Jeremie BoucherAbstract:Adipose tissue (AT) secretes several adipokines that influence insulin sensitivity and potentially link obesity to insulin resistance. Apelin, a peptide present in different tissues, is also secreted by adipocytes. Apelin is upregulated in obese and hyperinsulinemic humans and mice. Although a tight relation exists between the regulation of apelin and insulin, it remains largely unknown whether apelin affects whole-body Glucose Utilization. Herein, we show that in chowfed mice, acute intravenous injection of apelin has a powerful Glucose-lowering effect associated with enhanced Glucose Utilization in skeletal muscle and AT. Through in vivo and in vitro pharmacological and genetic approaches, we demonstrate the involvement of endothelial NO synthase, AMP-activated protein kinase, and Akt in apelin-stimulated Glucose uptake in soleus muscle. Remarkably, in obese and insulin-resistant mice, apelin restored Glucose tolerance and increased Glucose Utilization. Apelin could thus represent a promising target in the management of insulin resistance.