scholarly journals Brain Glucose Levels in Portacaval-Shunted Rats with Chronic, Moderate Hyperammonemia: Implications for Determination of Local Cerebral Glucose Utilization

1994 ◽  
Vol 14 (1) ◽  
pp. 113-124 ◽  
Author(s):  
Nancy F. Cruz ◽  
Gerald A. Dienel
Keyword(s):  
Glucose Utilization ◽  
Normal Values ◽  
Brain Structures ◽  
Glucose Content ◽  
Brain Glucose ◽  
Glucose Levels ◽  
Lumped Constant ◽  
Dg Method ◽  
The Brain

Rates of glucose utilization (lCMRglc) in many structures of the brain of fed, portacaval-shunted rats, when assayed with the [14C]deoxyglucose (DG) method in our laboratory, were previously found to be unchanged (30 of 36 structures) or depressed (6 structures) during the first 4 weeks after shunting, but to rise progressively to higher than normal values in 25 of 36 structures from 4–12 weeks. In contrast, lCMRglc, when assayed with the [14C]glucose method in another laboratory, was depressed in most structures of brains of 4–8-week shunted rats that had relatively high brain ammonia levels. There was a possibility that the increases in lCMRglc obtained with the [14C]DG method may have been artifactual, due, in part, to a change in brain glucose content which could alter the value of the lumped constant of the DG method. Brain glucose levels of shunted rats were, therefore, assayed by both direct chemical measurement in freeze-blown samples and by determination of steady-state brain:plasma distribution ratios for [14C]methylglucose; the methylglucose distribution ratio varies as a function of plasma and tissue glucose contents. Within a week after shunting, ammonia levels in blood and brain rose to 0.25–0.30 m M and 0.35–0.70 μmol/g, respectively, and mean plasma glucose levels fell from 9–10 m M to 7.4–8.5 m M, and then remained nearly constant. Brains of fedshunted rats had normal glycogen levels and stable but moderately reduced glucose contents between 1 and 12 weeks (i.e., 1.9–2.2 μmol/g). [14C]Methylglucose distribution ratios were essentially the same as those in controls in 22 brain structures at 2 and 8 weeks after shunting. Because brain glucose levels remained stable from 1 to 12 weeks after shunting, there is no evidence to support the hypothesis that the value of the lumped constant would have changed and caused an artifactual rise in lCMRglc.

scholarly journals The Deoxyglucose Method in the Ferret Brain. II. Glucose Utilization Images and Normal Values

1989 ◽  
Vol 9 (1) ◽  
pp. 43-52 ◽  
Author(s):  
C. Redies ◽  
M. Diksic ◽  
Y. L. Yamamoto
Keyword(s):  
Rate Constants ◽  
Glucose Utilization ◽  
Normal Values ◽  
Brain Size ◽  
Experimental Period ◽  
Brain Structures ◽  
Rate Limiting Step ◽  
Rate Limiting ◽  
The Brain ◽  
Deoxyglucose Method

To measure cerebral glucose utilization with the autoradiographic deoxyglucose method, the tracer transfer rate constants and lumped constants must be known. 2-Deoxyglucose (2-DG) and fluorodeoxyglucose (FDG) constants were determined in 18 gray and white matter brain structures of the anesthetized ferret. The ferret is a domestic carnivore particularly suitable for deoxyglucose studies because of its small brain size and low body weight. The average gray matter rate constants for tracer transfer across the blood-brain barrier are similar for 2-DG and FDG in the ferret brain ( K*1 = 0.21 ml/g/min and k*2 = 0.39 min−1). The rate constant for the rate-limiting step of tracer phosphorylation, k*3, is 1.6 times higher for FDG than for 2-DG (0.21 vs. 0.13 min−1). Loss of metabolized tracer is about 1–1.5%/min throughout the ferret brain for both tracers as estimated for a 180 min experimental period. Taking into account this loss, the lumped constant is 0.92 for FDG and 0.68 for 2-DG. Glucose utilization values in the brain of the anesthesized ferret range from 33 μmol/100 g/min in the corpus callosum to 104 μmol/100 g/min in the caudate nucleus. Representative glucose utilization images of coronal sections of the ferret brain are shown. Brain structures are identified on the same slices counterstained with thionin.

scholarly journals Influence of Glucose Supply and Demand on Determination of Brain Glucose Content with Labeled Methylglucose

1996 ◽  
Vol 16 (3) ◽  
pp. 439-449 ◽  
Author(s):  
Hajime Nakanishi ◽  
Nancy F. Cruz ◽  
Keiji Adachi ◽  
Louis Sokoloff ◽  
Gerald A. Dienel
Keyword(s):  
Glucose Level ◽  
Distribution Ratio ◽  
Plasma Glucose ◽  
Glucose Concentration ◽  
Surrounding Tissue ◽  
Metabolic Demand ◽  
Glucose Content ◽  
Brain Glucose ◽  
Glucose Levels

The equilibrium brain/plasma distribution ratio for 3- O-methyl-D-glucose (methylglucose) varies with plasma and tissue glucose contents and can be used to determine local glucose levels in brain. This ratio was previously found to rise as brain glucose concentration fell in response to lowered plasma glucose content. The ratios, however, differed with the same tissue glucose levels in conscious and pentobarbital-sedated rats, suggesting that changes in metabolic demand might alter the quantitative relationship between the methylglucose distribution ratio and brain glucose concentration. To examine this possibility, metabolic rate was varied by focal drug application, and hexose concentrations measured in treated and surrounding tissue. When tissue glucose levels were reduced by raised metabolic demand, methylglucose distribution ratios also fell. When brain glucose levels rose due to reduced consumption, the methylglucose distribution ratio also rose. Thus, in contrast to the inverse relationship between brain/plasma methylglucose ratio and brain glucose concentration when brain glucose content is altered secondarily to changes in plasma glucose level, changes in brain glucose content induced by altered glucose utilization cause the brain glucose level and methylglucose distribution ratio to rise and fall in a direct relationship. Determination of brain glucose content from methylglucose distribution ratios must take into account rates of glucose delivery and consumption.

scholarly journals Direct Measurement of the λ of the Lumped Constant of the Deoxyglucose Method in Rat Brain: Determination of λ and Lumped Constant from Tissue Glucose Concentration or Equilibrium Brain/Plasma Distribution Ratio for Methylglucose

1991 ◽  
Vol 11 (1) ◽  
pp. 25-34 ◽  
Author(s):  
Gerald A. Dienel ◽  
Nancy F. Cruz ◽  
Kentaro Mori ◽  
James E. Holden ◽  
Louis Sokoloff
Keyword(s):  
Plasma Glucose ◽  
Glucose Concentration ◽  
Full Range ◽  
Acid Extraction ◽  
Distribution Space ◽  
Glucose Levels ◽  
Lumped Constant ◽  
Distribution Spaces ◽  
The Brain

Steady-state distribution spaces of 2-[14C]deoxyglucose ([14C]DG), glucose, and 3- O-[14C]methylglucose at various concentrations of glucose in brain and plasma ranging from hypoglycemic to hyperglycemic levels have been determined by direct chemical analyses in the brains of conscious rats. The hexose concentrations were measured chemically in freeze-blown brain extracted with ethanol to avoid the degradation of acid-labile products of [14C]DG back to free [14C]DG that has been found to occur with the more commonly used perchloric acid extraction of brain. Corrections were also made for nonphosphorylatable, labeled products of [14C]DG found in the nonacidic fractions of the brain extracts, which were previously included with the assayed [14C]DG, and for the contribution of the hexose contents in the blood in the brain, which was found to be particularly critical for the determination of the glucose distribution space, especially in hypoglycemic states. From the measured contents of the hexoses in brain and plasma, the relationships of the tissue concentrations and distribution spaces of each of the hexoses and of the Λ (i.e., ratio of tissue distribution space of DG to that of glucose) of the DG method to the tissue glucose concentration were derived. The Λ was then quantitatively related to the measured equilibrium ratio for [14C]methylglucose over the full range of brain and plasma glucose levels. By combining these new data with the values for the lumped constant, the factor that converts rate of DG phosphorylation to glucose phosphorylation, previously determined in rats over the same range of plasma glucose levels, the phosphorylation coefficient was calculated and the lumped constant graphed as a function of the measured distribution space in brain for [14C]methylglucose.

scholarly journals Autoradiographic Determination of Regional Brain Glucose Content

1983 ◽  
Vol 3 (3) ◽  
pp. 303-310 ◽  
Author(s):  
Albert Gjedde ◽  
Nils Henrik Diemer
Keyword(s):  
Rat Brain ◽  
Brain Slices ◽  
Apparent Volume ◽  
Volume Of Distribution ◽  
Glucose Content ◽  
Brain Glucose ◽  
Lumped Constant ◽  
Normal Rat ◽  
Apparent Volume Of Distribution

Brain glucose content is an important experimental variable that affects the value of the “lumped constant” of the 2-deoxyglucose method. The apparent volume of distribution in brain of the nonmetabolizable glucose analog, 3- O-methylglucose, depends only on the glucose content. From the kinetic constants of glucose transport and the apparent volume of distribution, we used autoradiography to calculate the regional glucose content of the normal rat brain. The regional glucose content varied only insignificantly in gray matter regions; the average glucose content of all rat brain slices examined was 4 μmol g−1, with an average plasma glucose concentration of 8.6 m M. Regional values varied between 3.4 and 4.6 μmol g−1. Thus, there is no reason to believe that the regional values of the lumped constant vary significantly in normal rat brains.

scholarly journals Glucagon-Like Peptide-1 Decreases Intracerebral Glucose Content by Activating Hexokinase and Changing Glucose Clearance during Hyperglycemia

2012 ◽  
Vol 32 (12) ◽  
pp. 2146-2152 ◽  
Author(s):  
Michael Gejl ◽  
Lærke Egefjord ◽  
Susanne Lerche ◽  
Kim Vang ◽  
Bo Martin Bibby ◽  
...  
Keyword(s):  
Glucose Content ◽  
Brain Glucose ◽  
Glucose Levels ◽  
Hyperglycemic Clamp ◽  
Positron Emission ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Double Blinded ◽  
The Brain

Type 2 diabetes and hyperglycemia with the resulting increase of glucose concentrations in the brain impair the outcome of ischemic stroke, and may increase the risk of developing Alzheimer's disease (AD). Reports indicate that glucagon-like peptide-1 (GLP-1) may be neuroprotective in models of AD and stroke: Although the mechanism is unclear, glucose homeostasis appears to be important. We conducted a randomized, double-blinded, placebo-controlled crossover study in nine healthy males. Positron emission tomography was used to determine the effect of GLP-1 on cerebral glucose transport and metabolism during a hyperglycemic clamp with 18fluoro-deoxy-glucose as tracer. Glucagon-like peptide-1 lowered brain glucose ( P = 0.023) in all regions. The cerebral metabolic rate for glucose was increased everywhere ( P = 0.039) but not to the same extent in all regions ( P = 0.022). The unidirectional glucose transfer across the blood-brain barrier remained unchanged ( P = 0.099) in all regions, while the unidirectional clearance and the phosphorylation rate increased ( P = 0.013 and 0.017), leading to increased net clearance of the glucose tracer ( P = 0.006). We show that GLP-1 plays a role in a regulatory mechanism involved in the actions of GLUT1 and glucose metabolism: GLP-1 ensures less fluctuation of brain glucose levels in response to alterations in plasma glucose, which may prove to be neuroprotective during hyperglycemia.

scholarly journals Influence of Plasma Glucose Concentration on Lumped Constant of the Deoxyglucose Method: Effects of Hyperglycemia in the Rat

1990 ◽  
Vol 10 (6) ◽  
pp. 765-773 ◽  
Author(s):  
Franz Schuier ◽  
Francesco Orzi ◽  
Sumio Suda ◽  
Giovanni Lucignani ◽  
Charles Kennedy ◽  
...  
Keyword(s):  
Plasma Glucose ◽  
Glucose Concentration ◽  
Full Range ◽  
Brain Structures ◽  
Plasma Glucose Concentration ◽  
Glucose Levels ◽  
Lumped Constant ◽  
Arterial Plasma ◽  
The Brain ◽  
Deoxyglucose Method

The lumped constant of the deoxyglucose method was determined by the steady-state, model-independent method in the brain of normal conscious rats with arterial plasma glucose concentrations varying from normoglycemia (i.e., 8 m M) to hyperglycemia (i.e., 31 m M). The lumped constant for brain was found to decrease very gradually with increasing arterial plasma glucose concentration from a value of ∼0.45 in the midnor-moglycemic range (i.e., 7–8 m M) to ∼0.38 at 28–31 m M. 3- O-[14C]Methylglucose was used to assess the distribution of glucose within the brain structures in hyperglycemia; the results indicated that the glucose concentration, and therefore also the values for the lumped constant, remain relatively uniform in hyperglycemia with arterial plasma glucose concentrations as high as 34 m M. The values for the lumped constant for rat brain determined in the present studies were combined with those previously determined in this laboratory for hypoglycemia and normoglycemia by the same method to provide a single source for the values for the lumped constant to be used over the full range of arterial plasma glucose concentrations. In several rats the lumped constant for cephalic extracerebral tissues was also evaluated in parallel with those for the brain. The lumped constant for the cephalic extracerebral tissues was found to be about twice that for brain and to be unaffected by changes in arterial plasma glucose levels.

Rates of glucose utilization in brain of active and hibernating ground squirrels

1995 ◽  
Vol 268 (2) ◽  
pp. R445-R453 ◽  
Author(s):  
K. U. Frerichs ◽  
G. A. Dienel ◽  
N. F. Cruz ◽  
L. Sokoloff ◽  
J. M. Hallenbeck
Keyword(s):  
Glucose Utilization ◽  
Specific Activity ◽  
Ground Squirrels ◽  
Cold Adapted ◽  
Precursor Pool ◽  
Glucose Levels ◽  
Operational Equation ◽  
Dg Method ◽  
Deep Hibernation ◽  
Cerebral Structures

Rates of glucose utilization (CMRGlc) were determined in some cerebral structures of active warm- and cold-adapted ground squirrels and hibernating ground squirrels with [14C]deoxyglucose (DG) by direct chemical measurement of precursor and products in samples dissected from funnel-frozen brain. The rate of supply relative to demand of glucose and [14C]DG in brain of hibernating animals was similar to or greater than that of controls. [14C]DG cleared from the plasma in hibernators much more slowly than in active animals, and the level of unmetabolized [14C]DG in brain and the integrated specific activity of the precursor pool in plasma exceeded those of the active animals by 4- to 10-fold. At 45 min after an intravenous pulse of [14C]DG, the unmetabolized [14C]DG remaining in the brains of the hibernators accounted for approximately 96% of the total 14C compared with approximately 10-15% in the active animals. The value of lambda, a factor contained in the lumped constant of the operational equation of the [14C]DG method, was estimated for each animal and found to be relatively constant over the sixfold range of glucose levels in the brains of all animals. Calculated CMRGlc in squirrels in deep hibernation was only 1-2% of the values in active animals.

scholarly journals Chronic Dexamethasone Pretreatment Aggravates Ischemic Neuronal Necrosis

1986 ◽  
Vol 6 (4) ◽  
pp. 395-404 ◽  
Author(s):  
Tohru Koide ◽  
Tadeusz W. Wieloch ◽  
Bo K. Siesjö
Keyword(s):  
Brain Damage ◽  
Glucocorticoid Receptors ◽  
Neuronal Damage ◽  
Energy Charge ◽  
Cyclooxygenase Inhibitors ◽  
Brain Areas ◽  
Neuronal Necrosis ◽  
Brain Glucose ◽  
Glucose Levels ◽  
The Brain

This study addresses the question of whether the cyclooxygenase inhibitors indomethacin and diclofenac and the glucocorticosteroid dexamethasone ameliorate neuronal necrosis following cerebral ischemia. In addition, since these drugs inhibit the production of prostaglandins and depress phospholipase A2 activity, respectively, the importance of free fatty acids (FFAs) on the development of ischemic neuronal damage was assessed. Neuronal damage was determined in the rat brain at 1 week following 10 min of forebrain ischemia. The cyclooxygenase inhibitors, whether given before or after ischemia, failed to alter the brain damage incurred. Animals given dexamethasone were divided into three groups and the drug was administered at a constant dosage of 2 mg/kg: (a) 2 days, 1 day, and 3 h intraperitoneally before (chronic pretreatment), (b) 3 h intraperitoneally before (acute pretreatment), and (c) 5 min intravenously and 6 h and 1 day intraperitoneally after (chronic posttreatment) induction of ischemia. Acute pretreatment did not affect the histopathological outcome. Chronic posttreatment of animals with dexamethasone ameliorated the damage inflicted on the caudate nucleus, but had no effect on other brain areas investigated. Unexpectedly, the chronic pretreatment aggravated the brain damage and caused seizures following ischemia. Histopathological data showed massive neuronal damage in these brains. The accumulation of FFA levels during ischemia was markedly suppressed, and the decrease in the energy charge was curtailed by chronic pretreatment with dexamethasone. However, brain glucose levels in control animals and lactic acid concentrations following 10 min of ischemia were significantly higher both in the cerebral cortex and in the hippocampus of dexamethasone-treated animals. These results suggest that aggravation of neuronal necrosis by chronic dexamethasone pretreatment could be ascribed to lactic acidosis due to hyperglycemia in combination with an action of dexamethasone on glucocorticoid receptors in the brain.

Influence of current study load and examinations on the character of sympathetic-adrenal system reactions of students

1986 ◽  
Vol 67 (6) ◽  
pp. 436-438
Author(s):  
A. A. Kamaeva ◽  
M. V. Sukhanova ◽  
A. L. Braunagel ◽  
A. Ya. Kozhevnikova ◽  
S. S. Khaletova
Keyword(s):  
Blood Glucose ◽  
Educational Process ◽  
Glucose Content ◽  
Glucose Levels ◽  
Biochemical Effects ◽  
Blood Glucose Levels ◽  
Energy Needs ◽  
Simultaneous Study ◽  
Stimulation Of

The aim of this work was to study the urinary excretion of adrenaline and noradrenaline, blood glucose content and determination of skin temperature of students at different stages of the educational process. The simultaneous study of these indicators, in our opinion, is justified on the basis of biochemical effects of catecholamines-stimulation of glycogenolysis and lipolysis, increase in blood glucose levels, as well as its further use by tissues for energy needs.

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