Metabolism of Cysteine in Astroglial Cells: Synthesis of Hypotaurine and Taurine

Brand, Annette; Leibfritz, Dieter; Hamprecht, Bernd; Dringen, Ralf

doi:10.1046/j.1471-4159.1998.71020827.x

Cited by 71 publications

(51 citation statements)

References 26 publications

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“…This may suggest to us that L-cysteine may inhibit insulin release via a mechanism independent of H 2 S production and the resultant inhibition of glucose metabolism. For example, taurine, known to be produced from L-cysteine (35), was reported to inhibit glucose-induced insulin release from mouse islets (36).…”

Section: Fig 6 Effects Of L-cysteine and Nahs On Camentioning

confidence: 99%

l-Cysteine Inhibits Insulin Release From the Pancreatic β-Cell

et al. 2006

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Hydrogen sulfide (H 2 S) was historically recognized as a toxic gas generated by natural resources. However, its enzymatic production from L-cysteine has recently been demonstrated in mammals. Cystathionine ␤-synthase and cystathionine ␥-lyase, both of which can produce H 2 S, were expressed in mouse pancreatic islet cells and the ␤-cell line, MIN6. L-Cysteine and the H 2 S donor NaHS inhibited glucose-induced insulin release from islets and MIN6 cells. These inhibitory effects were reproduced when insulin release was stimulated by ␣-ketoisocaproate, tolbutamide, or high K ؉

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Section: Fig 6 Effects Of L-cysteine and Nahs On Camentioning

confidence: 99%

l-Cysteine Inhibits Insulin Release From the Pancreatic β-Cell

et al. 2006

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“…240 Surprisingly, only minor amounts of [3][4][5][6][7][8][9][10][11][12][13] C 1 ]cysteine are used as a substrate for glutathione synthesis, while hypotaurine and taurine are the major products of cysteine metabolism. 154 The reason for the lack in GLT synthesis from cysteine may be due to the preference of cystine for glial GSH synthesis. 241 Interestingly, inhibition of GLT formation increases taurine synthesis from extracellular cysteine.…”

Section: Other Biosynthetic Processes Contributing To Disposition Of mentioning

confidence: 99%

Regulation of glial metabolism studied by ¹³C‐NMR

Zwingmann¹,

Leibfritz²

2003

NMR in Biomedicine

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106

107

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Glial metabolism and their metabolic trafficking with neurons are essential parts of neuronal function, as they modulate, by this means, neuronal activity. Ex vivo and in vitro 13 C-NMR spectroscopy have been used to monitor neural cellular and tissue metabolism. Special emphasis has been given to the metabolic specialization of astrocytes and its enzymatic regulation. For this purpose primary cell cultures are useful tools to study neuronal-glial metabolic relationships as the extracellular fluid can be investigated and manipulated by various stimuli. In astrocytes, glucose is utilized predominantly anaerobically. Glycolysis is interrelated to the astrocytic TCA cycle via bi-directional signals and metabolic exchange processes between astrocytes and neurons. Besides glucose oxidation, neuronally released glutamate is metabolized through the glial TCA cycle. The flexibility of glutamate metabolism, depending on ammonia and energy homeostasis, and the discovered pyruvate recycling pathway in astrocytes, modulates the glutamine-glutamate cycle. 13 C-NMR studies have extended the concept of the 'non-stoichiometric' glutamate-glutamine cycle between neurons and astrocytes. An alanine-lactate shuttle between neurons and astrocytes contributes to nitrogen transfer from neurons to astrocytes, recycles energy substrates for neurons, and in return promotes intercellular glutamine-glutamate cycling. The conversion of alanine to lactate in astrocytes is regulated by intracytosolic pyruvate compartmentation. In essence, the metabolic flexibility and compartmentalized enzymatic specialization of astrocytes buffers the brain tissue against metabolic impairments and excitotoxicity in response to extracellular stimuli, some of them being released by neurons. These in vitro studies using 13 C-NMR spectroscopy provide important knowledge regarding physiological and pathophysiological regulation of neural metabolism to improve our understanding of general brain function.

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“…However, there is considerable confusion about chemical shifts of Tau in the literature. Two papers deserved special attention, one reporting the follow-up of L- [3][4][5][6][7][8][9][10][11][12][13] C]Cys metabolism in astrocytes (27) and the other analyzing the chemicophysical properties of hypotaurine (28). These papers attributed the downfield 13 C-upfield 1 H signal of Tau or hypotaurine to the C-1 CH 2 residue.…”

Section: Methodology Issuesmentioning

confidence: 99%

Methionine‐dependence phenotype of tumors: Metabolite profiling in a melanoma model using L‐[methyl‐¹³C]methionine and high‐resolution magic angle spinning ¹H–¹³C nuclear magnetic resonance spectroscopy

Morvan

Demidem

Guenin

et al. 2006

Magnetic Resonance in Med

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Tumors frequently have abnormal L-methionine (Met) metabolism, the so-called Met-dependence phenotype that refers to the inability to proliferate in the absence of Met. However, the origin of this phenotype is still unknown and may arise from one of several pathways of Met metabolism. To help characterize the metabolic features of Met-dependent/independent phenotypes, the fate of the methyl carbon of L-[methyl-

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Metabolism of Cysteine in Astroglial Cells: Synthesis of Hypotaurine and Taurine

Cited by 71 publications

References 26 publications

l-Cysteine Inhibits Insulin Release From the Pancreatic β-Cell

l-Cysteine Inhibits Insulin Release From the Pancreatic β-Cell

Regulation of glial metabolism studied by ¹³C‐NMR

Methionine‐dependence phenotype of tumors: Metabolite profiling in a melanoma model using L‐[methyl‐¹³C]methionine and high‐resolution magic angle spinning ¹H–¹³C nuclear magnetic resonance spectroscopy

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Metabolism of Cysteine in Astroglial Cells: Synthesis of Hypotaurine and Taurine

Cited by 71 publications

References 26 publications

l-Cysteine Inhibits Insulin Release From the Pancreatic β-Cell

l-Cysteine Inhibits Insulin Release From the Pancreatic β-Cell

Regulation of glial metabolism studied by 13C‐NMR

Methionine‐dependence phenotype of tumors: Metabolite profiling in a melanoma model using L‐[methyl‐13C]methionine and high‐resolution magic angle spinning 1H–13C nuclear magnetic resonance spectroscopy

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Product

Resources

About

Regulation of glial metabolism studied by ¹³C‐NMR

Methionine‐dependence phenotype of tumors: Metabolite profiling in a melanoma model using L‐[methyl‐¹³C]methionine and high‐resolution magic angle spinning ¹H–¹³C nuclear magnetic resonance spectroscopy