CONTROL OF GLYCOGEN LEVELS IN BRAIN<sup>1</sup>

Nelson, Stanley R.; Schulz, Demoy W.; Passonneau, Janet V.; Lowry, Oliver H.

doi:10.1111/j.1471-4159.1968.tb05904.x

Cited by 214 publications

(93 citation statements)

References 20 publications

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“…It is likely that in the previous study, total brain glycogen was even higher as animals experienced modest hyperglycemia (13−16 mM plasma glucose), which likely resulted in hyperinsulinemia. Thus, the concentrations of glycogen C1 may reflect the combined effect of elevated plasma glucose and/or insulin to promote net glycogen synthesis in the brain, which is in agreement with studies in cell cultures (Nelson et al, 1968;Swanson et al, 1989). Therefore, comparison of the glycogen C1 in this study with that in our previous study supports our previous assertion that glucose infusion resulted in net glycogen synthesis .…”

Section: Discussionsupporting

confidence: 91%

“…However, an endogenous store of carbohydrates, brain glycogen, can serve as an energy reserve when glucose supply is limited. The concentrations of brain glycogen can be influenced by glucose (Goldberg and O'Toole, 1969;Nelson et al, 1968), anesthetics (Nelson et al, 1968;Nordstrom and Siesjo, 1978) and neurotransmitters (Magistretti et al, 1986;Pellerin and Magistretti, 1994). It has also been suggested that brain glycogen metabolism may be affected by neuronal activity such as focal physiologic stimulation (Swanson, 1992).…”

Section: Introductionmentioning

confidence: 99%

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In vivo 13C NMR assessment of brain glycogen concentration and turnover in the awake rat

Choi

Gruetter

2003

Neurochemistry International

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Brain glycogen metabolism was recently observed in vivo and found to be very slow in the lightly ␣-chloralose anesthetized rat [J.Neurochem. 73 (1999) 1300]. Based on that slow turnover, the total glycogen content in the awake rat brain and its turnover time were assessed after administering 13 C-labeled glucose for 48 h. Label incorporation into glycogen, glucose, amino acid, and N-acetyl-aspartate (NAA) resonances was observed. The amount of 13 C label incorporated into glycogen was variable and did not correlate with that in glutamate (r = −0.1, P > 0.86). However, the amount of 13 C label incorporated into glycogen was very similar to that in NAA (r = 0.93), implying similar turnover times between brain glycogen and NAA (∼10 h). Absolute quantification of the total concentration of brain glycogen in the awake, normoglycemic rat yielded 3.3 ± 0.8 mol/g (n = 6, mean ± S.D.).

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

In vivo 13C NMR assessment of brain glycogen concentration and turnover in the awake rat

Choi

Gruetter

2003

Neurochemistry International

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“…40 Prolonged anesthesia with barbiturates and the administration of insulin lead to an increase in total brain glycogen content. 41 In the case of glucose feeding, the 13 C-labeling of glycogen C-1 (100.1 ppm) occurred already at the first day of feeding [ Fig. 3(A)] and showed a continuous increase during the following days.…”

Section: C-label Incorporation Into Cerebral Metabolitesmentioning

confidence: 99%

Feeding versus infusion: a novel approach to study the NAA metabolism in rat brain

et al. 2003

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Using in vivo 13 C-NMR spectroscopy, the energy metabolism in rat brain has commonly been studied via infusion of 13 C-labeled substrates on a minute to hour time scale. In the present study, as a novel approach, 13 C-enriched animal chow was administered over several days and compared with a 2 h infusion of [U-13 C 6 ]-glucose. Rats received chow containing either [U-13 C 6 ]-glucose or [U-13 C]-biomass (a mixture of proteins, lipids, DNA, and carbohydrates) during 3 to 5 days. During feeding with 13 C-labeled glucose and biomass, in vivo 13 C-NMR spectroscopy was carried out daily and revealed slow but successive label incorporation into a large number of metabolites. Lipids and proteins were not significantly 13 C-enriched during a 2 h infusion of 13 C-labeled glucose, but became the most prominent resonances in the 13 C feeding experiment. Likewise, feeding with 13 C-enriched biomass led to additional 13 C-label incorporation into creatine, urea carbons and glycogen. Finally, only the acetyl moiety of N-acetyl-aspartate (NAA) became significantly enriched during the 2 h infusion experiment, whereas the aspartyl moiety remained at natural abundance levels. In the feeding experiments, however, label incorporation into all carbons of NAA could be observed. Moreover, isotopomer analysis of brain extracts revealed that the acetyl moiety of NAA in feeding experiments was always more strongly 13 C-enriched than its aspartyl moiety, suggesting that the turnover of the acetyl moiety is faster than that of the aspartyl moiety. The different enrichment kinetics of acetyl and aspartyl moiety could be explained by the existence of two different metabolic pathways reflecting the compartmentalised synthesis of NAA.

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“…115,140,142 It has therefore been argued that small changes in brain lactate during stimulation are due to a futile cycling of glucose in and out of glycogen (brain glycogen shunt), 143 which would link brain glycogen metabolism to brain activity, even when brain glucose is not rate-limiting for metabolism. However, in the awake rat brain, extremely slow rates of bulk brain glycogen turnover were observed, 138 as illustrated in Fig.…”

Section: Brain Glycogen the Forgotten Energy Storementioning

confidence: 99%

Localized in vivo¹³C NMR spectroscopy of the brain

et al. 2003

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Localized 13C NMR spectroscopy provides a new investigative tool for studying cerebral metabolism. The application of 13 C NMR spectroscopy to living intact humans and animals presents the investigator with a number of unique challenges. This review provides in the first part a tutorial insight into the ingredients required for achieving a successful implementation of localized 13 C NMR spectroscopy. The difficulties in establishing 13 C NMR are the need for decoupling of the one-bond 13 C-1 H heteronuclear J coupling, the large chemical shift range, the low sensitivity and the need for localization of the signals. The methodological consequences of these technical problems are discussed, particularly with respect to (a) RF front-end considerations, (b) localization methods, (c) the low sensitivity, and (d) quantification methods. Lastly, some achievements of in vivo localized 13 C NMR spectroscopy of the brain are reviewed, such as: (a) the measurement of brain glutamine synthesis and the feasibility of quantifying glutamatergic action in the brain; (b) the demonstration of significant anaplerotic fluxes in the brain; (c) the demonstration of a highly regulated malate-aspartate shuttle in brain energy metabolism and isotope flux; (d) quantification of neuronal and glial energy metabolism; and (e) brain glycogen metabolism in hypoglycemia in rats and humans. We conclude that the unique and novel insights provided by 13 19-24 Most of these studies have involved the administration of a 13 C-enriched precursor. When the enriched 13 C label is transferred to molecules in the metabolic pathway, sensitivity can not only be increased, but important information on metabolic pathways can also be obtained. For example, recent studies showed that the information content of 13 C NMR spectroscopy can be amplified considerably, such as the resolved observation of GABA labeling in the human brain, as well as the first detection of lactate labeling in normal human brain. 8 In addition to its importance in assessing metabolism in intact brain, 13 C NMR spectroscopy has become an important and useful tool in assessing compartmentation of metabolism in brain cells using extracts. 25,26 In addition to its low sensitivity, 13 C NMR spectroscopy is methodologically more challenging than 1 H or even 31 P NMR spectroscopy. However, 13C NMR provides its own unique insight and advantages over 1 H NMR spectroscopy. The uniqueness of 13 C NMR stems mainly from its increased chemical shift dispersion, which can, for example, be used in two-dimensional NMR to increase spectral resolution following specific labeling of the protein. 27 As shall be elaborated further below, 13 C NMR spectroscopy in living tissue provides a unique window on in vivo metabolism as it occurs. In the

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CONTROL OF GLYCOGEN LEVELS IN BRAIN¹

Cited by 214 publications

References 20 publications

In vivo 13C NMR assessment of brain glycogen concentration and turnover in the awake rat

In vivo 13C NMR assessment of brain glycogen concentration and turnover in the awake rat

Feeding versus infusion: a novel approach to study the NAA metabolism in rat brain

Localized in vivo¹³C NMR spectroscopy of the brain

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CONTROL OF GLYCOGEN LEVELS IN BRAIN1

Cited by 214 publications

References 20 publications

In vivo 13C NMR assessment of brain glycogen concentration and turnover in the awake rat

In vivo 13C NMR assessment of brain glycogen concentration and turnover in the awake rat

Feeding versus infusion: a novel approach to study the NAA metabolism in rat brain

Localized in vivo13C NMR spectroscopy of the brain

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Product

Resources

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CONTROL OF GLYCOGEN LEVELS IN BRAIN¹

Localized in vivo¹³C NMR spectroscopy of the brain