Methionine-Induced Elevation of Plasma Homocysteine Concentration Is Associated with an Increase of Plasma Cholesterol in Adult Rats

Hirche, Frank; Schröder, Arlette; Knoth, Berit; Stangl, Gabriele I.; Eder, Klaus

doi:10.1159/000090635

Cited by 34 publications

(32 citation statements)

References 44 publications

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“…Our ¢nding that sulphur amino acid metabolites seem to interact with the lipid metabolism and lipid storage is in agreement with reports in rodent models (Anstee & Goldin 2006;Hirche, Schr˛der, Knoth, Stangl & Eder 2006;Zhan, Li, Xu & Zhao 2006). The reduced performance in ¢sh fed the plant-based test diets is most likely due to a reduced feed intake due to the di¡erent physical properties of the feeds as stated above.…”

Section: Discussionsupporting

confidence: 91%

Effect of taurine supplementation on the metabolism and body lipid-to-protein ratio in juvenile Atlantic salmon (Salmo salar)

Espe¹,

Ruohonen

El‐Mowafi

2011

Aquaculture Research

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Previously, we reported that methionine intake determined the taurine concentration in the liver of ongrowing Atlantic salmon fed plant protein diets. Further, the methionine intake and/or the increased taurine concentration following increased methionine intake a¡ected the liver lipid metabolism. The following study therefore aimed to test whether taurine a¡ected the growth or the type of growth when added in high plant protein diets naturally low in taurine but equal and adequate in dietary methionine. Juvenile Atlantic salmon [initial body weight (BW) of 2 g] were fed plant protein diets (16.5% ¢shmeal), which were supplemented with taurine or not for a period of 56 days. As a control for growth and normal metabolism, a ¢shmeal-based commercial diet (68% ¢shmeal) was used. Supplementation with taurine to high plant protein diets had a slightly negative e¡ect on weight gain, but the ¢nal body weight was not di¡erent. Interestingly, the pool of free amino acids in the liver and muscle was signi¢cantly higher in ¢sh fed the supplemented diet as compared with ¢sh fed the plant protein diet without taurine supplementation. Liver polyamine concentration was higher in ¢sh fed the supplemented diet than in ¢sh fed the similar diet without supplementation. Additionally, juvenile salmon fed the plant-based diet supplemented with taurine had a lower body lipidto-protein ratio due to a reduced whole-body lipid content, while the whole-body protein content was similar between treatments. Our study thus indicates that the addition of a low concentration of taurine to high plant protein diets interacts with lipid metabolism and storage, concomitantly a¡ecting the general metabolism as the concentrations of the free amino acids and polyamines in the liver were signi¢cantly higher. The possible reasons for these changes are discussed.

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Section: Discussionsupporting

confidence: 91%

Effect of taurine supplementation on the metabolism and body lipid-to-protein ratio in juvenile Atlantic salmon (Salmo salar)

Espe¹,

Ruohonen

El‐Mowafi

2011

Aquaculture Research

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“…Toward this goal, dietary supplementation with methionine itself may be considered. However, methionine is rapidly incorporated into protein, and it increases the plasma levels of homocysteine and cholesterol, which may be risk factors in cardiovascular diseases (Hirche et al, 2006). In fact, dietary methionine restriction, instead of supplementation, induces beneficial anti-aging effects (Malloy et al, 2006).…”

Section: Resultsmentioning

confidence: 99%

Methionine Sulfoxide Reductase A and a Dietary SupplementS-Methyl-L-Cysteine Prevent Parkinson's-Like Symptoms

Wassef¹,

Haenold²,

Hansel³

et al. 2007

J. Neurosci.

115

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Parkinson's disease (PD), a common neurodegenerative disease, is caused by loss of dopaminergic neurons in the substantia nigra. Although the underlying cause of the neuronal loss is unknown, oxidative stress is thought to play a major role in the pathogenesis of PD. The amino acid methionine is readily oxidized to methionine sulfoxide, and its reduction is catalyzed by a family of enzymes called methionine sulfoxide reductases (MSRs). The reversible oxidation-reduction cycle of methionine involving MSRs has been postulated to act as a catalytic antioxidant system protecting cells from oxidative damage. Here, we show that one member of the MSR family, MSRA, inhibits development of the locomotor and circadian rhythm defects caused by ectopic expression of human ␣-synuclein in the Drosophila nervous system. Furthermore, we demonstrate that one way to enhance the MSRA antioxidant system is dietary supplementation with S-methyl-L-cysteine (SMLC), found abundantly in garlic, cabbage, and turnips. SMLC, a substrate in the catalytic antioxidant system mediated by MSRA, prevents the ␣-synuclein-induced abnormalities. Therefore, interventions focusing on the enzymatic reduction of oxidized methionine catalyzed by MSRA represent a new prevention and therapeutic approach for PD and potentially for other neurodegenerative diseases involving oxidative stress.

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“…Treatment with vitamin B 12 , vitamin B 6 , and folic acid over 21 days significantly lowered homocysteine, but also TC, TG, and LDL plasma levels, in these individuals. Recently, it was shown that experimentally induced hyperhomocysteinemia in rats leads to significantly increased plasma cholesterol levels accompanied by an increased expression and activity of hepatic HMGCoA reductase, a rate-limiting enzyme in cholesterol biosynthesis [20][21][22] . In addition, it was demonstrated that homocysteine supplementation of yeast leads to an accumulation of S-adenosyl-homocysteine, which attenuates S-adenosyl-methionine-dependent methyltransferase activities and results in an inhibition of phospholipid methylation and finally triacylglycerol accumulation [23] .…”

Section: Discussionmentioning

confidence: 99%

The G Allele of Transcobalamin 2 c.776C→G Is Associated with an Unfavorable Lipoprotein Profile

Semmler

Farmand²,

Moskau³

et al. 2010

Ann Nutr Metab

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Background/Aim: Recent studies have suggested a relation of homocysteine with lipid metabolism. The aim of this study was to analyze a possible genetic basis for such a relation in 504 individuals including 135 consecutive Caucasian patients diagnosed with cerebrovascular disease as well as the patients’ healthy spouses (n = 100) and offspring (n = 269). Methods: We analyzed the association of plasma levels of lipoprotein(a), total cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL), and triglycerides with plasma homocysteine levels and with the following 7 variants of homocysteine metabolism: dihydrofolate reductase c.594 + 59del19bp, cystathionine β-synthase c.844_855ins68, methionine synthase c.2756A→G, methylenetetrahydrofolate reductase c.677C→T and c.1298A→C, reduced folate carrier 1 c.80G→A, and transcobalamin 2 (Tc2) c.776C→G. Results: Linear regression analysis showed an association of Tc2 c.776C→G with LDL (p = 0.010), HDL (p = 0.009), and TG (p = 0.007), with the G allele of Tc2 c.776C→G associated with an unfavorable blood lipid profile. Moreover, the G allele of Tc2 c.776C→G was associated with higher homocysteine plasma levels in the subgroup of patients (p = 0.013, 1-way ANOVA). Conclusion: These data support the hypothesis that alterations in homocysteine metabolism and an unfavorable blood lipoprotein profile may have a common genetic basis. Such conditions may be relevant for studies investigating independent risk factors for vascular disease.

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Methionine-Induced Elevation of Plasma Homocysteine Concentration Is Associated with an Increase of Plasma Cholesterol in Adult Rats

Cited by 34 publications

References 44 publications

Effect of taurine supplementation on the metabolism and body lipid-to-protein ratio in juvenile Atlantic salmon (Salmo salar)

Effect of taurine supplementation on the metabolism and body lipid-to-protein ratio in juvenile Atlantic salmon (Salmo salar)

Methionine Sulfoxide Reductase A and a Dietary SupplementS-Methyl-L-Cysteine Prevent Parkinson's-Like Symptoms

The G Allele of Transcobalamin 2 c.776C→G Is Associated with an Unfavorable Lipoprotein Profile

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