Pancreatic Hormones and Hepatic Methionine Adenosyltransferase in the Rat

Shou, Lien; Pan, Foo; Chin, Sing-fie

doi:10.3181/00379727-131-34029

Cited by 9 publications

(3 citation statements)

References 4 publications

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“…3D-G). In the methionine cycle, methionine adenosyltransferase catalyzes methionine and ATP into S-adenosyl methionine (SAM) ( 14 ) which acts as a universal methyl donor ( 15 ). DNA methyltransferases (DNMTs) transfer the methyl group to cytosine and convert SAM to S-adenosyl homocysteine (SAH) which is further degraded to homocysteine (HCY) by SAH hydrolase ( 16 ).…”

Section: Resultsmentioning

confidence: 99%

Maternal obesity may disrupt offspring metabolism by inducing oocyte genome hyper-methylation via increased DNMTs

Chao,

Lu,

et al. 2024

Preprint

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Maternal obesity has deleterious effects on oocyte genome methylation establishment, yet the underlying mechanisms remain unclear. In the present study, we first find that maternal obesity induced by high-fat diet (HFD) disturbs genomic methylation in oocytes, and at least a part of the altered methylation is transmitted to F2 oocytes and livers via females. We further identified that altered metabolites such as methionine and melatonin may play a key role in the re-methylation establishment in oocytes of obese mice. Exogenous melatonin treatment significantly reduces the hyper-methylation of HFD oocytes. The higher expression of DNMT3a and DNMT1 in HFD oocytes is also decreased by melatonin supplement, which may be mediated by cAMP/PKA/CREB pathway. These results suggest that maternal obesity-induced genomic methylation alterations in oocytes, can be partly transmitted to F2 in females, and that melatonin is involved in regulating the hyper-methylation of HFD oocytes via increasing the expression of DNMTs mediated by cAMP/PKA/CREB pathway.

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Section: Resultsmentioning

confidence: 99%

Maternal obesity may disrupt offspring metabolism by inducing oocyte genome hyper-methylation via increased DNMTs

Chao,

Lu,

et al. 2024

Preprint

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“…It serves as a universal methyl donor for a class of enzymes known as methyltransferases (MTases), which catalyze the transfer of methyl groups to biomolecules such as DNA, RNA, protein, and other metabolites that require them, as reviewed previously [ 66 , 67 ]. SAM is synthesized from methionine and ATP via the enzyme methionine adenosyltransferase (MAT), also called S-adenosyl methionine synthase [ 74 ]. SAM is a crucial precursor to the anti-inflammatory polyamines spermidine and spermine [ 75 ].…”

Section: Folate B12 and The Methionine Cyclementioning

confidence: 99%

The Role of Methyl Donors of the Methionine Cycle in Gastrointestinal Infection and Inflammation

Vaccaro

Naser

2021

Healthcare

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Vitamin deficiency is well known to contribute to disease development in both humans and other animals. Nonetheless, truly understanding the role of vitamins in human biology requires more than identifying their deficiencies. Discerning the mechanisms by which vitamins participate in health is necessary to assess risk factors, diagnostics, and treatment options for deficiency in a clinical setting. For researchers, the absence of a vitamin may be used as a tool to understand the importance of the metabolic pathways in which it participates. This review aims to explore the current understanding of the complex relationship between the methyl donating vitamins folate and cobalamin (B12), the universal methyl donor S-adenosyl-L-methionine (SAM), and inflammatory processes in human disease. First, it outlines the process of single-carbon metabolism in the generation of first methionine and subsequently SAM. Following this, established relationships between folate, B12, and SAM in varying bodily tissues are discussed, with special attention given to their effects on gut inflammation.

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“…During this reaction, L-methyltetrahydrofolate donates a methyl group to homocysteine using B 12 as a cofactor [ 15 ]. The methionine generated this way can subsequently be incorporated into protein or adenosylated to generate S-adenosyl methionine (SAM), which is the universal methyl donor and precursor to polyamine biosynthesis [ 16 , 17 ].…”

Section: Introductionmentioning

confidence: 99%

Folate and Vitamin B12 Deficiency Exacerbate Inflammation during Mycobacterium avium paratuberculosis (MAP) Infection

2023

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Folate and vitamin B12 deficiency is highly prevalent among Crohn’s disease (CD) patients. Furthermore, CD pathology can be mediated by Mycobacterium avium subsp. paratuberculosis (MAP) infection. However, the direct effect of folate (B9) and cobalamin (B12) deficiency during MAP infection remains uncharacterized. This study investigates how folate and B12 deficiency impedes macrophage apoptosis and exacerbates the inflammation in macrophages infected with MAP isolated from CD patients. Accordingly, we measured folate and B12 in ex vivo plasma samples collected from CD patients with or without MAP infection (N = 35 per group). We also measured the expression of the pro-inflammatory cytokines IL-1β and TNF-α, cellular apoptosis and viability markers, and bacterial viability in MAP-infected macrophages cultured in folate and B12 deficient media. We determined that MAP-positive CD patients have significantly lower plasma folate and B12 in comparison to MAP-negative CD patients [414.48 ± 94.60 pg/mL vs. 512.86 ± 129.12 pg/mL, respectively]. We further show that pro-inflammatory cytokines IL-1β and TNF-α are significantly upregulated during folate and vitamin B12 deprivation following MAP infection by several folds, while supplementation significantly reduces their expression by several folds. Additionally, depletion of folate, B12, and folate/B12 following MAP infection, led to decreased macrophage apoptosis from 1.83 ± 0.40-fold to 1.04 ± 0.08, 0.64 ± 0.12, and 0.45 ± 0.07 in folate-low, B12-low, and folate/B12-low cells, respectively. By contrast, folate and folate/B12 supplementation resulted in 3.38 ± 0.70 and 2.58 ± 0.14-fold increases in infected macrophages. Interestingly, changes in overall macrophage viability were only observed in folate-high, folate/B12-high, and folate/B12-low media, with 0.80 ± 0.05, 0.82 ± 0.02, and 0.91 ± 0.04-fold changes, respectively. Incubation of Caco-2 intestinal epithelial monolayers with supernatant from infected macrophages revealed that folate/B12 deficiency led to increased LDH release independent of oxidative stress. Overall, our results indicate that folate and B12 are key vitamins affecting cell survival and inflammation during MAP infection.

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Pancreatic Hormones and Hepatic Methionine Adenosyltransferase in the Rat

Cited by 9 publications

References 4 publications

Maternal obesity may disrupt offspring metabolism by inducing oocyte genome hyper-methylation via increased DNMTs

Maternal obesity may disrupt offspring metabolism by inducing oocyte genome hyper-methylation via increased DNMTs

The Role of Methyl Donors of the Methionine Cycle in Gastrointestinal Infection and Inflammation

Folate and Vitamin B12 Deficiency Exacerbate Inflammation during Mycobacterium avium paratuberculosis (MAP) Infection

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