Betaine supplementation decreases plasma homocysteine in healthy adult participants: a meta-analysis

McRae, Marc P.

doi:10.1016/j.jcm.2012.11.001

Cited by 39 publications

(31 citation statements)

References 33 publications

(51 reference statements)

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“…Supplementation of either folate or betaine have the capacity to lower plasma homocysteine (Keser et al, 2013;McRae, 2013) and fasting plasma homocysteine shows a strong inverse relationship with plasma folate. Moreover, post methionine load levels of homocysteine have a strong inverse relationship with plasma betaine (Holm, 2004), which is in keeping with the theory that BHMT functions to dispose of excess methionine.…”

Section: Regulation Of Homocysteine Metabolismmentioning

confidence: 99%

Methionine metabolism in Yucatan miniature swine

McBreairty

2016

Appl. Physiol. Nutr. Metab.

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Methionine Metabolism in Yucatan Miniature SwineMethionine is an essential amino acid which when not incorporated into protein, can be converted to S-adenosylmethionine, the universal methyl donor in over 200 transmethylation reactions, that include creatine and phosphatidylcholine (PC) synthesis, as well as deoxyribonucleic acid (DNA) methylation. Following transmethylation, homocysteine is formed which can be converted to cysteine via transsulfuration or remethylated to methionine by receiving a methyl group from folate or betaine. Changes to methyl group availability in utero can lead to permanent changes in epigenetic patterns of DNA methylation which has been implicated in "fetal programming," a phenomenon associated with poor nutrition during fetal development that results in low birth weight and disease in later life. It has been shown that programming can also occur in the neonate. So our global objective was to understand how the variability of nutrients involved in methionine metabolism can affect methionine and methyl group availability.We hypothesize that nutrients that converge on methionine metabolism can affect methionine availability for its various functions. In this thesis, we used intrauterine growth restricted (IUGR) piglets to investigate whether a global nutritional insult in utero can lead to a perturbed methionine metabolism. Our results demonstrate that IUGR piglets have a lower capacity to dispose of homocysteine via both transsulfuration and remethylation pathways, as well as a lower incorporation of methyl groups into PC. The second objective of this thesis was to determine whether variation in methionine supply and demand can affect methionine availability. We demonstrated that stimulating either iii acute or chronic creatine synthesis leads to lower methyl incorporation into protein and PC in pigs. Furthermore, when methionine is limiting, supplementation with either folate or betaine leads to higher methionine availability for protein synthesis. Lastly, because creatine is increasingly being utilized as an ergogenic and neuroprotective supplement, we wanted to determine whether provision of the creatine precursor, guanidinoacetate (GAA), could effectively increase tissue creatine stores. We showed that 2.5 weeks of supplementation with GAA is more effective than creatine at increasing hepatic and muscle creatine stores. The results of this thesis demonstrate that the presence of IUGR, an increased demand for creatine synthesis or the supplementation with remethylation nutrients can each affect methionine availability; all are important when considering neonatal nutrient requirements. Furthermore, although GAA is effective at increasing levels of tissue creatine, higher GAA methylation can limit methionine availability for growth and synthesis of PC.iv

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Section: Regulation Of Homocysteine Metabolismmentioning

confidence: 99%

Methionine metabolism in Yucatan miniature swine

McBreairty

2016

Appl. Physiol. Nutr. Metab.

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“…The recommended betaine intake is estimated at 0.5 to 3 grams per day [111][112][113]. Homocysteine is methylated to methionine with either betaine or L-5-methyl-THF as the methyl donor.…”

Section: Betainementioning

confidence: 99%

“…Thus, betaine and L-5-methyl-THF are interchangeable sources of methyl group in the conversion of homocysteine to methionine [110]. The reaction that uses betaine as a methyl donor is catalyzed by the enzyme BHMT (betaine-homocysteine methyltransferase), which is located only in the liver and kidney [112,114,115]. In the liver, BHMT catalyzes up to 50% of homocysteine metabolism [112].…”

Section: Betainementioning

confidence: 99%

“…The reaction that uses betaine as a methyl donor is catalyzed by the enzyme BHMT (betaine-homocysteine methyltransferase), which is located only in the liver and kidney [112,114,115]. In the liver, BHMT catalyzes up to 50% of homocysteine metabolism [112]. Therefore, BHMT regulates homocysteine levels in the liver.…”

Section: Betainementioning

confidence: 99%

“…Therefore, BHMT regulates homocysteine levels in the liver. Epidemiological studies have indicated that dietary supplementation with betaine may reduce homocysteine levels in healthy volunteers and individuals with hyperhomocysteinemia [112,114]. Studies have shown that treatment with betaine may reduce the risk of consequences of severe MTHFR deficiency [116].…”

Section: Betainementioning

confidence: 99%

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Women with Methylenetetrahydrofolate Reductase Gene Polymorphism and the Need for Proper Periconceptional Folate Supplementation

Sullivan¹,

Murray²,

Assefa³

2015

JPP

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Maternal folate supplementation is critical for fetal development. Women with MTHFR (methylenetetrahydrofolate reductase) gene polymorphisms may not be getting the proper folate form to support fetal development. The objectives of this review were to: (1) undertake a comprehensive review on the association of MTHFR polymorphisms with the risk for various congenital diseases and other adverse pregnancy outcomes, (2) assess the efficacy and safety of current folic acid and other supplementations in women with the MTHFR polymorphism, and (3) provide guidance on the appropriate supplementation for women of childbearing potential with the MTHFR gene polymorphism in order to decrease these adverse pregnancy outcomes. Our assessments show that women with MTHFR gene polymorphism cannot efficiently convert folic acid to L-5-methyl-tetrahydofolate, the predominant active form of folic acid, due to reduced MTHFR enzymatic activity. L-5-methyl-tetrahydrofolate is currently commercially available under several brand names. Based on our comprehensive review and knowledge of the biochemistry of the folates, we recommend that L-5-methyltetrahydrofolate be given in combination with folic acid to women with MTHFR polymorphism that are pregnant or planning to become pregnant. Further study is needed to determine the optimal dose.

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Betaine ameliorates doxorubicin‐induced cardiomyopathy by inhibiting oxidative stress, inflammation, and fibrosis through the modulation of AMPK/Nrf2/TGF‐β expression

Singh,

Yadav,

Patel

et al. 2024

Environmental Toxicology

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Doxorubicin (DOX) is a broad‐spectrum antibiotic with potent anti‐cancer activity. Nevertheless, despite having effective anti‐neoplasm activity, its use has been clinically restricted due to its life‐threatening side effects, such as cardiotoxicity. It is evident that betaine has anti‐oxidant, and anti‐inflammatory activity and has several beneficial effects, such as decreasing the amyloid‐β generation, reducing obesity, improving steatosis and fibrosis, and activating AMP‐activated protein kinase (AMPK). However, whether betaine could mitigate DOX‐induced cardiomyopathy is still unexplored. Cardiomyopathy was induced in male Sprague Dawley rats using DOX (4 mg/kg dose with a cumulative dose of 20 mg/kg, i.p.). Further, betaine (200 and 400 mg/kg) was co‐treated with DOX through oral gavage for 28 days. After the completion of the study, several biochemical, oxidative stress parameters, histopathology, western blotting, and qRT‐PCR were performed. Betaine treatment significantly reduced CK‐MB, LDH, SGOT, and triglyceride levels, which are associated with cardiotoxicity. DOX‐induced increased oxidative stress was also mitigated by betaine intervention as the SOD, catalase, MDA, and nitrite levels were restored. The histopathological investigation also confirmed the cardioprotective effect of betaine against DOX‐induced cardiomyopathy as the tissue injury was reversed. Further, molecular analysis revealed that betaine suppressed the DOX‐induced increased expression of phospho‐p53, phospho‐p38 MAPK, NF‐kB p65, and PINK 1 with an upregulation of AMPK and downregulation of Nrf2 expression. Interestingly, qRT‐PCR experiments show that betaine treatment alleviates the DOX‐induced increase in inflammatory (TNF‐α, NLRP3, and IL‐6) and fibrosis (TGF‐β and Acta2) related gene expression, halting the cardiac injury. Interestingly, betaine also improves the mRNA expression of Nrf2, thus modulating the expression of antioxidant proteins and preventing oxidative damage. Here, we provide the first evidence that betaine treatment prevents DOX‐induced cardiomyopathy by inhibiting oxidative stress, inflammation, and fibrosis by regulating AMPK/Nrf2/TGF‐β expression. We believe that betaine can be utilized as a potential novel therapeutic strategy for preventing DOX‐induced cardiotoxicity.

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Betaine supplementation decreases plasma homocysteine in healthy adult participants: a meta-analysis

Cited by 39 publications

References 33 publications

Methionine metabolism in Yucatan miniature swine

Methionine metabolism in Yucatan miniature swine

Women with Methylenetetrahydrofolate Reductase Gene Polymorphism and the Need for Proper Periconceptional Folate Supplementation

Betaine ameliorates doxorubicin‐induced cardiomyopathy by inhibiting oxidative stress, inflammation, and fibrosis through the modulation of AMPK/Nrf2/TGF‐β expression

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