Restriction of dietary methyl donors limits methionine availability and affects the partitioning of dietary methionine for creatine and phosphatidylcholine synthesis in the neonatal piglet

Robinson, Jason L.; McBreairty, Laura E.; Randell, Edward; Brunton, Janet A.; Bertolo, Robert F.

doi:10.1016/j.jnutbio.2016.07.001

Cited by 22 publications

(19 citation statements)

References 34 publications

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“…Sevoflurane can disrupt methionine and cysteine metabolism, increasing beta‐amyloid and tau levels, eventually leading to neurological damage. Conversely, impaired remethylation of homocysteine (Robinson et al, 2016) also causes neurodevelopmental disorders (Jadavji et al, 2014. In rats, in addition to abnormal methylation, sevoflurane affected arginine/proline metabolism (Jiang et al, 2017).…”

Section: Oxidative Stressmentioning

confidence: 99%

“…Sevoflurane can disrupt methionine and cysteine metabolism, increasing beta-amyloid and tau levels, eventually leading to neurological damage. Conversely, impaired remethylation of homocysteine (Robinson et al, 2016) also causes neurodevelopmental disorders (Jadavji et al, 2014. In rats, in addition to abnormal methylation, sevoflurane affected arginine/proline metabolism (Jiang et al, 2017). Arginine metabolism has been associated with neurodevelopment (Wu et al, 2009) and neurological diseases (Basso and Pennuto, 2015) and proline may affect tau turnover (Yamada et al, 2015).…”

Section: Abnormal Methylationmentioning

confidence: 99%

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Fundamentals of fetal toxicity relevant to sevoflurane exposures during pregnancy

Chai

Cheng

Jiang³

2018

Intl J of Devlp Neuroscience

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Over the last three decades, advances in medical and surgical techniques have proven life saving and life‐improving for young children. Consequently, early and repeated exposure to general anesthetics in childhood has increased. However, accumulating evidence suggests that general anesthetics may be neurotoxic in children. Of particular concern is the neurotoxicity fetuses may suffer from maternal exposure to sevoflurane during surgeries and fetal intervention procedures performed during the second trimester, as this can cause neurodevelopmental impairment in offspring. In this review we demonstrate that the pathology associated with fetal toxicity resulting from exposure to sevoflurane during pregnancy involves oxidative stress, neuroinflammation, neuroapoptosis, and alteration of synaptic properties. The mechanisms remain to be elucidated, but may include increased tau protein phosphorylation and abnormal methylation. These findings highlight the need for a global and comprehensive understanding of the potential neurotoxicity of anesthetic exposure in fetuses and its long‐term effects.

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Section: Oxidative Stressmentioning

confidence: 99%

Section: Abnormal Methylationmentioning

confidence: 99%

Fundamentals of fetal toxicity relevant to sevoflurane exposures during pregnancy

Chai

Cheng

Jiang³

2018

Intl J of Devlp Neuroscience

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“…How Met or TSAA requirements are partitioned into their different roles throughout the life span of mammals remains to be investigated but is the focus of ongoing research. Interestingly, in a mini‐pig model, an 80% dietary MetR had no effect on hepatic protein synthesis, and thus a portion of the requirement of Met that has been quantified in many species may in part be to supply methyl groups, which exemplifies the importance of reporting the dietary intake of these compounds. In methyl transfer reactions, SAM will transfer its methyl group to a variety of acceptors for the synthesis of products, such as creatine from guanidinoacetate and phosphatidylcholine from phosphatidylethanolamine .…”

Section: Dietary Considerations For the Control Of Transmethylation mentioning

confidence: 99%

“…The methyl‐accepting compounds include homocysteine, creatine, choline, and carnitine and, when supplemented in the diet, result in a decreased need for donors, improved energy and macronutrient metabolism, and improved physical and developmental outcomes. When chemically defined diets were fed to growing piglets (8 days old), the dietary methyl donors supplied were either deficient or sufficient, and Met was limited to 80% of requirements, the methyl‐deficient diet resulted in lower plasma concentrations of plasma choline, betaine, and folate and greater homocysteine than the methyl‐sufficient group . Furthermore, the methyl‐deficient diet resulted in greater phosphatidylcholine synthesis and lower creatine synthesis, but hepatic protein synthesis and DNA and protein methylation were unchanged .…”

Section: Dietary Considerations For the Control Of Transmethylation mentioning

confidence: 99%

Lessons from animal nutritionists: dietary amino acid requirement studies and considerations for healthy aging studies

Shoveller

McKnight²,

Wood

et al. 2018

Annals of the New York Academy of Sciences

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Dietary restriction (DR) increases median life span and protects against age-related disease. Improved longevity can be achieved by restriction of dietary energy, protein, or amino acids (AAs), such as methionine (Met). Met requirements have been defined using methodologies that measure the dose response to Met when all other dietary variables are held constant and with outcomes focused on protein turnover. Here, we cover protein and sulfur AA requirements and discuss the terms "deficient," "optimal," and "excess" and how these need to be considered. We additionally discuss the effect of methyl-donating compounds on sulfur AA metabolism and outcomes. We will discuss how the mechanistic target of rapamycin complex 1 (mTORC1) signaling network regulates protein turnover, lipogenesis and cell growth, proliferation, differentiation, and metabolism in response to hormones, AAs, and cellular energy status. Inhibition of mTORC1 signaling with rapamycin or genetic mutation increases median life span in model organisms, and mTORC1 inhibition may be responsible for some of the life span-extending effects of DR. Finally, we discuss how the sulfur AAs may regulate aspects of reactive oxygen species (ROS) mitigation. Overall, we suggest that approaches evaluating AA intake need to consider whole-body protein synthesis and measures related to tissue-specific and whole-body metabolism that have been associated with longevity.

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“…In terms of amino acid methylation, abnormal methylation of amino acid disturbed cysteine/methionine metabolism. In cysteine/methionine metabolism, Chung and Li suggested that the deceasing of S‐Adenosylmethionine up‐regulated the homocysteine level, which accelerated neuropathology of neurodegenerative disorders by increasing beta‐amyloid and Tau levels(Li et al, 2014; Chung et al, 2016); on the other hand, impaired remethylation of homocysteine resulted from abnormal methylation prevented homocysteine translating into methionine (Robinson et al, 2016) which is often accompanied by neurodevelopmental disorders (Jadavji Nafisa et al, 2014). As shown in Fig.…”

Section: Introductionmentioning

confidence: 99%

Potential neurotoxicity of prenatal exposure to sevoflurane on offspring: Metabolomics investigation on neurodevelopment and underlying mechanism

Jiang

Li²,

Wang

et al. 2017

Intl J of Devlp Neuroscience

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Repeated or prolonged anesthesia to pregnant women disturbs neurodevelopment of developing infants, but its mechanism has not been elaborated absolutely. This study was conducted to investigate the mechanism of potential neurotoxicity on their offspring generation after sevoflurane anesthesia in adult animals during pregnancy based on metabolomics. 16 pregnant rats were equally assigned to sevoflurane group and control group, and serum samples were collected from their 7-day-old offspring for metabolomics analysis using ultra performance liquid chromatography coupled to time-of-flight mass spectrometry. Principal component analysis and partial least squares-discriminate analysis were used for pattern recognition, and pathway analysis was performed by MetaboAnalyst platform. 29 metabolites were discovered as neurotoxicity related-biomarkers, among which S-Adenosylmethioninamine was inhibited dramatically after sevoflurane exposure. Prenatal exposure to sevoflurane led to a significant reduction in S-Adenosylmethionine level, as shown by enzyme-linked immunosorbent assay. Pathway analysis highlighted that prenatal exposure to sevoflurane induced alteration in arginine/proline metabolism, cysteine/methionine metabolism, and so on. The most important altered metabolic pathway was arginine/proline metabolism. This study suggests that abnormal methylation and disturbed arginine/proline metabolism may crucially contribute to the mechanism with neurotoxicity on offspring generation after sevoflurane anesthesia in adult animals during pregnancy, and dietary supplement of S-Adenosylmethionine and modulating arginine/proline metabolism may be the potential therapeutic targets for protecting neurodevelopment from detrimental effects of prenatal exposure to inhalational anesthetics.

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Restriction of dietary methyl donors limits methionine availability and affects the partitioning of dietary methionine for creatine and phosphatidylcholine synthesis in the neonatal piglet

Cited by 22 publications

References 34 publications

Fundamentals of fetal toxicity relevant to sevoflurane exposures during pregnancy

Fundamentals of fetal toxicity relevant to sevoflurane exposures during pregnancy

Lessons from animal nutritionists: dietary amino acid requirement studies and considerations for healthy aging studies

Potential neurotoxicity of prenatal exposure to sevoflurane on offspring: Metabolomics investigation on neurodevelopment and underlying mechanism

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