Lack of effect of oral choline supplement on the concentrations of choline metabolites in human brain

Tan, Jeannie; Blüml, Stefan; Hoang, Tuan; Dubowitz, David J.; Mevenkamp, Gregor; Ross, Brian D.

doi:10.1002/mrm.1910390619

Cited by 35 publications

(24 citation statements)

References 11 publications

(23 reference statements)

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“…The choline (Cho) signal on MRS is comprised of a group of components including free choline, phosphorylcholine, and phosphatidylcholine which constitute brain myelin and allow fluidity of cell membranes [41,42]. However, the complete metabolite profile contributing to the Cho signal is not certain [43].…”

Section: Mrs-based Central Nervous System Biochemical Analysismentioning

confidence: 99%

The in-depth evaluation of suspected mitochondrial disease

Haas

Parikh

Falk

et al. 2008

Molecular Genetics and Metabolism

313

300

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Mitochondrial disease confirmation and establishment of a specific molecular diagnosis requires extensive clinical and laboratory evaluation. Dual genome origins of mitochondrial disease, multiorgan system manifestations, and an ever increasing spectrum of recognized phenotypes represent the main diagnostic challenges. To overcome these obstacles, compiling information from a variety of diagnostic laboratory modalities can often provide sufficient evidence to establish an etiology. These include blood and tissue histochemical and analyte measurements, neuroimaging, provocative testing, enzymatic assays of tissue samples and cultured cells, as well as DNA analysis. As interpretation of results from these multifaceted investigations can become quite complex, the Diagnostic Committee of the Mitochondrial Medicine Society developed this review to provide an overview of currently available and emerging methodologies for the diagnosis of primary mitochondrial disease, primarily focusing on disorders characterized by impairment of oxidative phosphorylation. The aim of this work is to facilitate the diagnosis of mitochondrial disease by geneticists, neurologists, and other metabolic specialists who face the challenge of evaluating patients of all ages with suspected mitochondrial disease.

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Section: Mrs-based Central Nervous System Biochemical Analysismentioning

confidence: 99%

The in-depth evaluation of suspected mitochondrial disease

Haas

Parikh

Falk

et al. 2008

Molecular Genetics and Metabolism

313

300

View full text Add to dashboard Cite

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“…59,80 The total observable Cho concentration in the human brain has been measured at 1-2 mM, with approximately 0.6 mM of PC and 1.0 mM of GPC. [81][82][83][84] Cho is required for the synthesis of both the neurotransmitter acetylcholine and the phospholipid phosphatidylcholine (Figure 3). Although acetylcholine is produced only by cholinergic neurons, phosphatidylcholine is produced in all cells as a major membrane constituent.…”

Section: Impaired Phospholipid Metabolism In Bipolar Disordermentioning

confidence: 99%

Mitochondrial dysfunction in bipolar disorder: evidence from magnetic resonance spectroscopy research

2005

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Magnetic resonance spectroscopy (MRS) affords a noninvasive window on in vivo brain chemistry and, as such, provides a unique opportunity to gain insight into the biochemical pathology of bipolar disorder. Studies utilizing proton ( 1 H) MRS have identified changes in cerebral concentrations of N-acetyl aspartate, glutamate/glutamine, choline-containing compounds, myo-inositol, and lactate in bipolar subjects compared to normal controls, while studies using phosphorus ( 31 P) MRS have examined additional alterations in levels of phosphocreatine, phosphomonoesters, and intracellular pH. We hypothesize that the majority of MRS findings in bipolar subjects can be fit into a more cohesive bioenergetic and neurochemical model of bipolar illness that is both novel and yet in concordance with findings from complementary methodological approaches. In this review, we propose a hypothesis of mitochondrial dysfunction in bipolar disorder that involves impaired oxidative phosphorylation, a resultant shift toward glycolytic energy production, a decrease in total energy production and/or substrate availability, and altered phospholipid metabolism. Molecular Psychiatry (2005) 10, 900-919.

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“…From MRS studies on tissues in vivo, the choline signal is primarily observed as a prominent singlet at 3.2 ppm that includes contributions from free choline, GPC and PC, and is often referred to as 'total choline' (38)(39)(40). In the present study, we obtained high resolution signals of Cho, PC and GPC at the chemical shifts 3.19, 3.21 and 3.22 ppm, respectively.…”

Section: Discussionmentioning

confidence: 66%

Metabolic characteristics of acute necrotizing pancreatitis and chronic pancreatitis

Tian

Wang

et al. 2012

Mol Med Report

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Abstract. The etiology and pathogenesis of pancreatitis remains unclear. In the presence of pancreatic inflammation, metabolite abnormalities appear before transformation of tissue structure and changes in functions occur. Detection of abnormalities in metabolite levels facilitates a greater understanding of the pathophysiological events and aids in the early diagnosis of the disease. In this study, metabolic profiles from the pancreas of Wistar rats were examined using high-resolution proton magic angle spinning nuclear magnetic resonance (MAS NMR) spectroscopy to investigate the metabolite indicator(s) of acute necrotizing pancreatitis (ANP) and chronic pancreatitis (CP). The animals were divided into three groups: those with histologically confirmed ANP (n=7), those with CP (n=6) and a control group (n=9). The processed NMR spectra were analyzed using principal component analysis (PCA) to extract characteristic metabolites of ANP and CP. Levels of leucine, isoleucine and valine were increased in the ANP group, whereas an opposite trend was observed in the CP group. Increases in phosphocholine, glycerophosphocholine and choline levels, and decreases in fatty acids, lactate, betaine and glycine levels were observed in both the ANP and CP groups. Additionally, the lipid content in the CP group was higher than that observed in the ANP group. An increase in taurine levels was observed only in the CP group. In conclusion, pancreatitis causes a disruption of the metabolism in the pancreas at a molecular level, with increased taurine levels being a potential metabolite indicator for those with CP.

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Lack of effect of oral choline supplement on the concentrations of choline metabolites in human brain

Cited by 35 publications

References 11 publications

The in-depth evaluation of suspected mitochondrial disease

The in-depth evaluation of suspected mitochondrial disease

Mitochondrial dysfunction in bipolar disorder: evidence from magnetic resonance spectroscopy research

Metabolic characteristics of acute necrotizing pancreatitis and chronic pancreatitis

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