In vivo and in vitro proton NMR spectroscopic studies of thiamine-deficient rat brains

Lee, Haakil; Holburn, George E.; Price, Ronald R.

doi:10.1002/1522-2586(200102)13:2<163::aid-jmri1025>3.0.co;2-z

Cited by 19 publications

(22 citation statements)

References 30 publications

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“…The selective effect of thiamine deficiency on neuronal integrity, that is, the NAA peak, observed herein with selectively bred rats of Wistar stock contrasts with prior MRS studies of thiamine deficiency conducted in SpragueDawley rats (Lee et al, 2001(Lee et al, , 1995. Both of those two longitudinal studies found a significant decline in the Cho/ NAA ratio soon after a regimen of pyrithiamine injections, followed by dose-dependent recovery with thiamine replenishment.…”

Section: Neurochemical Basis Of Tissue Recoverycontrasting

confidence: 69%

“…Both of those two longitudinal studies found a significant decline in the Cho/ NAA ratio soon after a regimen of pyrithiamine injections, followed by dose-dependent recovery with thiamine replenishment. The later study (Lee et al, 2001) confirmed the in vivo results with in vitro analysis and concluded that a determinant of the neuroanatomical lesions of WE relates to a deficit in Cho compounds. To address the discrepancy between the results of the Lee et al (2001Lee et al ( , 1995 studies and the present study, group differences were re-examined using the Cho/NAA ratio but no differences related to treatment were detected.…”

Section: Neurochemical Basis Of Tissue Recoverysupporting

confidence: 53%

“…The later study (Lee et al, 2001) confirmed the in vivo results with in vitro analysis and concluded that a determinant of the neuroanatomical lesions of WE relates to a deficit in Cho compounds. To address the discrepancy between the results of the Lee et al (2001Lee et al ( , 1995 studies and the present study, group differences were re-examined using the Cho/NAA ratio but no differences related to treatment were detected. Whether the difference in study results is related to prior alcohol exposure or differences in experimental protocols, scanning parameters, or rat strains remains unresolved.…”

Section: Neurochemical Basis Of Tissue Recoverymentioning

confidence: 62%

“…Initial MRI studies, conducted at 1.5 T, used thiamine deficiency models of WE (Pentney et al, 1993) and reported increased volume of lateral ventricles followed by normalization with a thiamine-enriched diet (Acara et al, 1995). Such neuropathology is accelerated with the dietary thiamine antagonist, pyrithiamine (Langlais and Savage, 1995;Langlais and Zhang, 1997;Lee et al, 2001Lee et al, , 1995. Glucose administration to rats made thiamine deficient with pyrithiamine treatment produced impairment of the bloodbrain barrier, observed on T1-weighted images (used for tissue depiction) collected at high scanner field strength (4.7 T) (Zelaya et al, 1995), and hyperintensities in the hippocampus as well as in the thalamus, hypothalamus, collicular bodies, observed on T2-weighted images (used for fluid depiction), that endured for at least 1 month (Jordan et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

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Development and Resolution of Brain Lesions Caused by Pyrithiamine- and Dietary-Induced Thiamine Deficiency and Alcohol Exposure in the Alcohol-Preferring Rat: A Longitudinal Magnetic Resonance Imaging and Spectroscopy Study

Pfefferbaum

Adalsteinsson

Bell

et al. 2006

Neuropsychopharmacol

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Wernicke's encephalopathy (WE) is characterized by lesions in thalamus, hypothalamus (including mammillary nuclei), and inferior colliculi, results in serious disabilities, has an etiology of thiamine deficiency, is treatable with thiamine, and occurs most commonly with alcoholism. Despite decades of study, whether alcohol exposure exacerbates the neuropathology or retards its resolution remains controversial. To examine patterns of brain damage and recovery resulting from thiamine deprivation with and without alcohol exposure, we conducted in vivo magnetic resonance imaging (MRI) and magnetic resonance spectroscopy (MRS) at 3 T in alcohol-preferring (P) rats, which had voluntarily consumed large amounts of alcohol before thiamine manipulation. A total of 18 adult male P rats (nine alcohol-exposed) received a thiamine-deficient diet for 2 weeks: 10 (five alcohol-exposed) received intraperitoneal (i.p.) pyrithiamine (PT) and eight (four alcohol-exposed) received i.p. thiamine supplementation. Neurological signs developed by day 14. Rats were scanned before thiamine depletion and 18 and 35 days after thiamine repletion. Two-dimensional J-resolved MRS single-voxel spectra with water reference were collected in a voxel subtending the thalamus; metabolite quantification was corrected for voxel tissue content. MRI identified significant enlargement of dorsal ventricles and increase in signal intensities in thalamus, inferior colliculi, and mammillary nuclei of PT compared with thiamine-treated (TT) groups from MRI 1-2, followed by significant normalization from MRI 2-3 in thalamus and colliculi, but not mammillary nuclei and lateral ventricles. Voxel-by-voxel analysis revealed additional hyperintense signal clusters in the dorsal and ventral hippocampus and enlargement of the fourth ventricle. MRS showed a significant decline and then partial recovery in thalamic N-acetylaspartate, a marker of neuronal integrity, in PT compared with TT rats, with no change detected in creatine, choline, or glutamate. PT rats with prior alcohol exposure exhibited attenuated recovery in the thalamus and arrested growth of the corpus callosum; further, two of the five alcohol-exposed PT rats died prematurely. Parenchymal and ventricular changes with thiamine manipulation concur with human radiological signs of WE. The enduring macrostructural and neurochemical abnormalities involving critical nodes of Papez circuit carry liabilities for development of amnesia and incomplete recovery from other cognitive and motor functions subserved by the affected neural systems.

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Section: Neurochemical Basis Of Tissue Recoverycontrasting

confidence: 69%

Section: Neurochemical Basis Of Tissue Recoverysupporting

confidence: 53%

Section: Neurochemical Basis Of Tissue Recoverymentioning

confidence: 62%

Section: Introductionmentioning

confidence: 99%

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Development and Resolution of Brain Lesions Caused by Pyrithiamine- and Dietary-Induced Thiamine Deficiency and Alcohol Exposure in the Alcohol-Preferring Rat: A Longitudinal Magnetic Resonance Imaging and Spectroscopy Study

Pfefferbaum

Adalsteinsson

Bell

et al. 2006

Neuropsychopharmacol

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“…9 Betaine is an important metabolite functioning both as an osmolyte to protect against osmotic stress and a methyl group donor. 9,15 Hence, glucose was chosen to probe glycolysis and the Krebs cycle, while glycine was chosen to probe betaine, which is trimethylglycine, a catabolic product of glycine. 14 Therefore, the major goal of this study was to establish baseline distributions of metabolites derived from U-13 C-glucose and 2-13 C-glycine over oyster tissues by using 13 C NMR measurement and to demonstrate the feasibility of using NMR for that purpose.…”

Section: Introductionmentioning

confidence: 99%

Assessment of Metabolism of the Eastern Oyster and Eastern Elliptio Using NMR Spectroscopy

Lee¹

2016

J. Braz. Chem. Soc.

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Metabolites are known to characterize the functional responses of a cell. Therefore, a quantitative measurement of metabolite profiles can provide insight into the underlying effect of genetic or environmental actions on cell metabolism. It follows then that the study of the metabolite profiles of bivalve mollusks, such as oysters, can be particularly worthwhile in assessing changes in physiology, pharmacology and toxicology that result from their adaptation to changing environments. We have determined the metabolic profiles of three different organ groups in freshwater mussel and oysters by using 1 H (proton) and 13 C (carbon) NMR (nuclear magnetic resonance) spectroscopy following the infusion of 13 C glucose or 13 C glycine, respectively. The result shows infused glucose formed glycogen by glycogen synthesis, alanine by glycolysis, and glutamate and aspartate through the Krebs cycle and glycine formed serine by the glycine cleavage system in oysters. Decrease in adenosine triphosphate (ATP), glucogen, putrescine and ornithine were observed in the fasting state freshwater mussel. Our result opens the possibility that organ specific metabolic fingerprints can be established to interpret functional adaptations to environmental and nutritional challenges using NMR spectroscopy.

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Proton MR spectroscopic studies of chronic alcohol exposure on the rat brain

Lee

Holburn

Price

2003

Magnetic Resonance Imaging

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Purpose: To better understand the long-term pathophysiologic mechanisms of alcoholism-related organic brain damage by serially assessing brain metabolites in chronically exposed rats using both in vivo magnetic resonance spectroscopy (MRS) and high-resolution nuclear magnetic resonance (NMR) from brain extracts. Materials and Methods:The alcoholic regimen was continued up to 60 weeks. In vivo proton MRS studies were performed at 200 MHz using a small animal imaging/spectrometer. In vitro rat brain extracts were also examined using a 500 MHz vertical bore magnet. Comparison measurements were also obtained in an age-matched control group. Results:In vivo results showed that there is a significant increase in the Cho/NAA ratio in the chronic alcohol-exposed group that reached a maximum around 16 weeks. After 44 weeks of alcohol exposure, Cho/NAA in the alcohol group decreased significantly from its maximum value to a value that was significantly lower than those from the control groups. Brain extract studies demonstrated that PC and GPC were the main components responsible for the observed in vivo spectral changes after 16 and 60 weeks of alcohol consumption, respectively. Conclusion:The fluctuation of choline-containing metabolites during alcohol intoxication could explain sometimes seemingly conflicting and confusing results from MRS studies in human and animal studies in which the duration of alcohol consumption and amount are varied widely.

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In vivo and in vitro proton NMR spectroscopic studies of thiamine-deficient rat brains

Cited by 19 publications

References 30 publications

Development and Resolution of Brain Lesions Caused by Pyrithiamine- and Dietary-Induced Thiamine Deficiency and Alcohol Exposure in the Alcohol-Preferring Rat: A Longitudinal Magnetic Resonance Imaging and Spectroscopy Study

Development and Resolution of Brain Lesions Caused by Pyrithiamine- and Dietary-Induced Thiamine Deficiency and Alcohol Exposure in the Alcohol-Preferring Rat: A Longitudinal Magnetic Resonance Imaging and Spectroscopy Study

Assessment of Metabolism of the Eastern Oyster and Eastern Elliptio Using NMR Spectroscopy

Proton MR spectroscopic studies of chronic alcohol exposure on the rat brain

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