Effect of Insulin on the Synthesis of Glycogen in Cerebral Cortical Slices of Alloxan Diabetic Rats

Prasannan, K. G.; Subrahmanyam, K

doi:10.1210/endo-82-1-1

Cited by 37 publications

(9 citation statements)

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“…For this set of nerves the control population incubated for 60 min in normal aCSF contained 4.85 Ϯ 0.31 pmol of glycogen/ g of protein (n ϭ 6). In other preparations exposure to high glucose concentration increases glycogen content (Prasannan and Subrahmanyam, 1966;Swanson et al, 1989b;Dringen and Hamprecht, 1992), whereas exposure to norepinephrine causes glycogen content to fall (Quach et al, 1978;Magistretti, 1988;Magistretti et al, 1993). Incubation of nerves in 25 mM glucose for 60 min induced an increase in glycogen stores to 7.90 Ϯ 0.59 pmol of glycogen/ g of protein (n ϭ 6; p Ͻ 0.001 vs control); conversely, pretreatment for 60 min with 1 mM norepinephrine led to a decline in RON glycogen (2.56 Ϯ 0.08 pmol of glycogen/ g of protein; n ϭ 7; p Ͻ 0.01 vs control).…”

Section: Glycogen Content Of Ronmentioning

confidence: 99%

Astrocytic Glycogen Influences Axon Function and Survival during Glucose Deprivation in Central White Matter

Wender

Brown²,

Fern³

et al. 2000

J. Neurosci.

340

339

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We tested the hypothesis that astrocytic glycogen sustains axon function during and enhances axon survival after 60 min of glucose deprivation. Axon function in the rat optic nerve (RON), a CNS white matter tract, was monitored by measuring the area of the stimulus-evoked compound action potential (CAP). Switching to glucose-free artificial CSF (aCSF) had no effect on the CAP area for ϳ30 min, after which the CAP rapidly failed. Exposure to glucose-free aCSF for 60 min caused irreversible injury, which was measured as incomplete recovery of the CAP. Glycogen content of the RON fell to a low stable level 30 min after glucose withdrawal, compatible with rapid use in the absence of glucose. An increase of glycogen content induced by high-glucose pretreatment increased the latency to CAP failure and improved CAP recovery. Conversely, a decrease of glycogen content induced by norepinephrine pretreatment decreased the latency to CAP failure and reduced CAP recovery. To determine whether lactate represented the fuel derived from glycogen and shuttled to axons, we used the lactate transport blockers quercetin, ␣-cyano-4-hydroxycinnamic acid (4-CIN), and p-chloromercuribenzene sulfonic acid ( pCMBS). All transport blockers, when applied during glucose withdrawal, decreased latency to CAP failure and decreased CAP recovery. The inhibitors 4-CIN and pCMBS, but not quercetin, blocked lactate uptake by axons. These results indicated that, in the absence of glucose, astrocytic glycogen was broken down to lactate, which was transferred to axons for fuel. Key words: astrocytes; ␣-cyano-4-hydroxycinnamate; glucose; hypoglycemia; lactate; p-chloromercuribenzene sulfonic acid; quercetin; rat optic nerveThe function of brain glycogen is not well understood. Glycogen turns over rapidly in the brain, however, and turnover is enhanced when adjacent neural activity is increased (Orkand et al., 1973;Pentreath and Kai-Kai, 1982;Swanson et al., 1992). It is appealing to imagine that glycogen might serve to provide fuel to the brain when glucose is in short supply. Indeed, astrocytic glycogen in vitro is degraded rapidly when glucose is withdrawn (Dringen et al., 1993), and glycogen falls rapidly in vivo during ischemia, with a time course that is closely related to the depletion of ATP and the accumulation of lactate (Swanson et al., 1989a). These observations are consistent with the action of glycogen as a fuel source during glucose shortage, but they do not prove this hypothesis. Glycogen content varies by a factor of two or more between brain regions [it is highest in the brainstem and cerebellum and lowest in the striatum and white matter (Swanson et al., 1989a)]. Energy metabolism also varies significantly between different brain regions (Sokoloff et al., 1977). Therefore, glycogen could be more protective against glucose depletion in some areas than in others.Given all of the above, it is natural to wonder whether glycogen can enhance the survival and function of brain tissue in the absence of glucose. Surprisingly, only a single st...

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Section: Glycogen Content Of Ronmentioning

confidence: 99%

Astrocytic Glycogen Influences Axon Function and Survival during Glucose Deprivation in Central White Matter

Wender

Brown²,

Fern³

et al. 2000

J. Neurosci.

340

339

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“…Although the activity of glucose-6-phosphatase is reported to be low in mammalian brain [20,21,44,431, it apparently produces a significant hydrolysis of FDG-6-P04 to FDG, which is then available for rephosphorylation (k;) or clearance into the blood (k:). Our extension of Sokoloff's model has been derived 1231 to include the hydrolysis reaction mediated by the rate constant kf (see Fig 1 and Eq.…”

Section: Kennedy Et Al [261 From Measurements In 2 Rhesusmentioning

confidence: 99%

“…An advantage of this analog over labeled glucose is that the end-product of phosphorylation (DG-or FDG-6-P04) is trapped in the tissue and released with a very slow clearance. This is because DG-or FDG-6-P04 cannot be metabolized further [53], DG-or FDG-6-P04 has a low membrane permeability, and glucose-6-phosphatase (which can hydrolyze the 6-PO, form to DG or FDG) exhibits low activity levels in brain [20,21,44,451. This trapping mechanism provides an excellent means for development and application of analytical models for the measurement of CMRGlc with PCT.…”

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confidence: 99%

Tomographic measurement of local cerebral glucose metabolic rate in humans with (F‐18)2‐fluoro‐2‐deoxy‐D‐glucose: Validation of method

Phelps

Huang

Hoffman

et al. 1979

Annals of Neurology

2,202

1,062

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Tracer techniques and quantitative autoradiographic and tissue counting models for measurement of metabolic rates were combined with positron computed tomography (PCT) and (F-18)2-fluoro-2-deoxy-D-glucose (FDG) for the measurement of local cerebral metabolic rate for glucose (LCMRGlc) in humans. A three-compartment model, which incorporates hydrolysis of FDG-6-PO4 to FDG, was developed for the measure of kinetic constants and calculation of LCMRGlc. Our model is an extension of that developed by Sokoloff et al. Although small, hydrolysis of FDG-6-PO4 was found to be significant. A PCT system, the ECAT, was used to determine the rate constants, lumped constant, and stability of the model in human beings. The data indicate that cerebral FDG-6-PO4 in humans increases for about 90 minutes, plateaus, and then slowly decreases. After 10 minutes, cerebral blood FDG activity levels were found to be a minor fraction of tissue activity. Precursor pool turnover rate, distribution volumes, and red blood cell-plasma concentration ratios were determined. Reproducibility (precision) of LCMRGlc measurements (approximate 2 cm2 regions) was +/- 5.5% over a 5-hour period. The replacement of arterial blood sampling with venous sampling was validated.

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“…On the other hand, the values of the kinetic rate constants for DG and FDG in humans are very similar, suggesting that these two analogues of glucose have similar affinities for the facilitated transport system and are similar as sub strates for hexokinase in the brain. Phosphatase activity in mammalian brain is low (Hers and DeDuve, 1950;Hers, 1957;Raggi et al, 1960;Prasannan and Subrahmanyan, 1968). A negligible error is produced by not including phos phatase activity in the model, i.e., by omitting kt the kinetic rate constant for phosphatase activity.…”

Section: Kinetic Rate Constantsmentioning

confidence: 99%

Use of 2-Deoxy-D[1-¹¹C]Glucose for the Determination of Local Cerebral Glucose Metabolism in Humans: Variation within and between Subjects

Reivich

Alavi

Wolf

et al. 1982

J Cereb Blood Flow Metab

128

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tracer for the measurement of LCMRgl and to determine its variability within subjects over a 2-h period. The kinetic rate constants for ll C-deoxyglucose were determined for gray and white matter and found to be very similar to those for 18F-fluorodeoxyglucose, suggesting that these two analogues of glu cose have similar affinities for the facilitated transport system and are similar substrates for hexokinase in the brain. The coefficient of variation of repeated measurements of LCMRgl in a series of six normal subjects was 5.5% to S.7% for various gray matter structures and 9.7% to 14.0% for white matter struc tures. The pattern of cerebral metabolic rates is relatively constant in a given individual when the conditions of the study are unchanged. The ability to make repeat measurements in the same subject reduces the variance due to between-subject differences, allowing smaller changes in LCMRgl to be de tected with confidence. Key Words: Coefficient of variation for repeat determinations-Deoxyglucose-Kinetic rate constants-Local cerebral glu cose metabolism.The 14C-2-deoxyglucose method for measuring local cerebral glucose metabolism (LCMRgl) in animals is a widely accepted technique that employs the autoradiographic determination of radioactivity concentration in tissues and allows quantitation of

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Effect of Insulin on the Synthesis of Glycogen in Cerebral Cortical Slices of Alloxan Diabetic Rats

Cited by 37 publications

References 0 publications

Astrocytic Glycogen Influences Axon Function and Survival during Glucose Deprivation in Central White Matter

Astrocytic Glycogen Influences Axon Function and Survival during Glucose Deprivation in Central White Matter

Tomographic measurement of local cerebral glucose metabolic rate in humans with (F‐18)2‐fluoro‐2‐deoxy‐D‐glucose: Validation of method

Use of 2-Deoxy-D[1-¹¹C]Glucose for the Determination of Local Cerebral Glucose Metabolism in Humans: Variation within and between Subjects

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Effect of Insulin on the Synthesis of Glycogen in Cerebral Cortical Slices of Alloxan Diabetic Rats

Cited by 37 publications

References 0 publications

Astrocytic Glycogen Influences Axon Function and Survival during Glucose Deprivation in Central White Matter

Astrocytic Glycogen Influences Axon Function and Survival during Glucose Deprivation in Central White Matter

Tomographic measurement of local cerebral glucose metabolic rate in humans with (F‐18)2‐fluoro‐2‐deoxy‐D‐glucose: Validation of method

Use of 2-Deoxy-D[1-11C]Glucose for the Determination of Local Cerebral Glucose Metabolism in Humans: Variation within and between Subjects

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Use of 2-Deoxy-D[1-¹¹C]Glucose for the Determination of Local Cerebral Glucose Metabolism in Humans: Variation within and between Subjects