Plasma total homocysteine levels in hyperthyroid and hypothyroid patients

Nedrebø, Bjørn Gunnar; Ericsson, Ulla-Britt; Nygård, Ottar; Refsum, Helga; Ueland, Per Magne; Aakvaag, A.; Aanderud, Sylvi; Lien, Ernst A.

doi:10.1016/s0026-0495(98)90198-6

Cited by 124 publications

(68 citation statements)

References 22 publications

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“…Methionine Transport-Methionine transport into isolated hepatocytes was measured as described by Salter et al (29). Following a 20-min preincubation period, [1][2][3][4][5][6][7][8][9][10][11][12][13][14] C]methionine was added to a final concentration of 0.5 mM (0.2 Ci). At 5, 35, 65, 95, and 125 s following the addition of methionine, 1-ml aliquots were transferred to 1.5-ml microcentrifuge tubes containing 0.25 ml of silicone oil mixture (2:1 (v/v) Dow Corning 550 silicone oil and dinonyl phthalate) layered on top of 0.1 ml of 6% (v/v) perchloric acid.…”

Section: Methodsmentioning

confidence: 99%

“…Increased Flux through Transsulfuration following Glucagon-The second step of the transsulfuration pathway involves the cleavage of cystathionine to produce cysteine, NH 4 ϩ , and ␣-ketobutyrate. Incubating cells with L- [1-14 C]methionine will give rise to ␣-[1-…”

Section: In Vivo Effects Of Glucagon On Homocysteine Metabolismmentioning

confidence: 99%

“…Homocysteine has several possible fates: 1) remethylation to form methionine via either the cobalamin-dependent methionine synthase (using N 5 -methyltetrahydrofolate as a methyl donor) or betaine:homocysteine methyltransferase (using betaine as a methyl donor); 2) catabolism by the transsulfuration pathway, ultimately forming cysteine; 3) export to the extracellular space. Two vitamin B 6 -dependent enzymes comprise the transsulfuration pathway: cystathionine ␤-synthase, which condenses homocysteine with serine to form cystathionine, and cystathionine ␥-lyase, which cleaves cystathionine to cysteine, NH 4 ϩ , and ␣-ketobutyrate.…”

mentioning

confidence: 99%

“…In recent years it has also become apparent that certain hormones can affect homocysteine metabolism. It has been shown that hypothyroid patients tend to have elevated plasma homocysteine and that these levels are normalized when thyroid levels are restored by thyroxine treatment (4,5). Estrogen therapy for post-menopausal women has been shown to lower plasma homocysteine (6).…”

mentioning

confidence: 99%

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Hyperglucagonemia in Rats Results in Decreased Plasma Homocysteine and Increased Flux through the Transsulfuration Pathway in Liver

Jacobs¹,

Stead²,

Brosnan

et al. 2001

Journal of Biological Chemistry

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An elevated plasma level of homocysteine is a risk factor for the development of cardiovascular disease. The purpose of this study was to investigate the effect of glucagon on homocysteine metabolism in the rat. Male Sprague-Dawley rats were treated with 4 mg/kg/day (3 injections per day) glucagon for 2 days while control rats received vehicle injections. Glucagon treatment resulted in a 30% decrease in total plasma homocysteine and increased hepatic activities of glycine N-methyltransferase, cystathionine ␤-synthase, and cystathionine ␥-lyase. Enzyme activities of the remethylation pathway were unaffected. The 90% elevation in activity of cystathionine ␤-synthase was accompanied by a 2-fold increase in its mRNA level. Hepatocytes prepared from glucagon-injected rats exported less homocysteine, when incubated with methionine, than did hepatocytes of saline-treated rats. Flux through cystathionine ␤-synthase was increased 5-fold in hepatocytes isolated from glucagon-treated rats as determined by production of 14 CO 2 and ␣-[1-14 C]ketobutyrate from L-[1-14 C]methionine. Methionine transport was elevated 2-fold in hepatocytes isolated from glucagon-treated rats resulting in increased hepatic methionine levels. Hepatic concentrations of S-adenosylmethionine and S-adenosylhomocysteine, allosteric activators of cystathionine ␤-synthase, were also increased following glucagon treatment. These results indicate that glucagon can regulate plasma homocysteine through its effects on the hepatic transsulfuration pathway.An elevated plasma concentration of homocysteine, a sulfurcontaining amino acid derived from methionine, has been recognized as an independent risk factor for the development of vascular disease (1). Methionine is adenylated by methionine adenosyltransferase to form S-adenosylmethionine, an important biological methyl donor. Numerous methyltransferases catalyze the transfer of a methyl group from S-adenosylmethionine to a methyl acceptor, producing a methylated product and S-adenosylhomocysteine, which is subsequently hydrolyzed to form adenosine and homocysteine. Homocysteine has several possible fates: 1) remethylation to form methionine via either the cobalamin-dependent methionine synthase (using N 5 -methyltetrahydrofolate as a methyl donor) or betaine:homocysteine methyltransferase (using betaine as a methyl donor); 2) catabolism by the transsulfuration pathway, ultimately forming cysteine; 3) export to the extracellular space. Two vitamin B 6 -dependent enzymes comprise the transsulfuration pathway: cystathionine ␤-synthase, which condenses homocysteine with serine to form cystathionine, and cystathionine ␥-lyase, which cleaves cystathionine to cysteine, NH 4 ϩ , and ␣-ketobutyrate.Altered flux through the remethylation or transsulfuration pathways as a result of genetic mutations or impaired vitamin status has been shown to affect plasma homocysteine levels (2, 3). In recent years it has also become apparent that certain hormones can affect homocysteine metabolism. It has been shown that hypothyroid ...

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Section: Methodsmentioning

confidence: 99%

Section: In Vivo Effects Of Glucagon On Homocysteine Metabolismmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Hyperglucagonemia in Rats Results in Decreased Plasma Homocysteine and Increased Flux through the Transsulfuration Pathway in Liver

Jacobs¹,

Stead²,

Brosnan

et al. 2001

Journal of Biological Chemistry

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“…27 Hypothyroidism, via an unclear mechanism, can raise Hcy by an average of 5.8 umol/l compared with euthyroid controls. 28 In systemic lupus erythematosus, Hcy ≥ 14.1 umol/l is an independent risk factor for arterial thrombosis. 29 Pernicious anemia elevates Hcy by causing cobalamine deficiency.…”

Section: Etiology Of Hyperhomocysteinemiamentioning

confidence: 99%

The association of homocysteine and coronary artery disease

Gauthier¹,

Keevil²,

McBride³

2003

Clinical Cardiology

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Summary: Hyperhomocysteinemia has been associated with increased risk of atherosclerosis and myocardial infarction by a number of prospective case-control studies. A variety of genetic mutations, nutritional deficiencies, disease states, and drugs can elevate homocysteine concentrations. Treatment with folic acid with or without B-complex vitamins effectively lowers homocysteine levels. Whether therapy corresponds with decreased risk of coronary events is unknown, but may be promising. This article reviews the biochemistry of homocysteine metabolism, pathogeneisis, and etiology of hyperhomocysteinemia, along with its association with coronary artery disease, screening, and treatment.

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Nonfasting Plasma Total Homocysteine Levels and All-Cause and Cardiovascular Disease Mortality in Elderly Framingham Men and Women

Bostom

Silbershatz²,

Rosenberg³

et al. 1999

Arch Intern Med

279

146

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Background: Elevated fasting total homocysteine (tHcy) levels were recently shown to confer an independent risk for all-cause and cardiovascular disease (CVD) mortality among selected Norwegian patients with confirmed coronary heart disease. We examined whether elevated fasting plasma tHcy levels were predictive of all-cause and CVD mortality in a large, population-based sample of elderly US women and men.

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Plasma total homocysteine levels in hyperthyroid and hypothyroid patients

Cited by 124 publications

References 22 publications

Hyperglucagonemia in Rats Results in Decreased Plasma Homocysteine and Increased Flux through the Transsulfuration Pathway in Liver

Hyperglucagonemia in Rats Results in Decreased Plasma Homocysteine and Increased Flux through the Transsulfuration Pathway in Liver

The association of homocysteine and coronary artery disease

Nonfasting Plasma Total Homocysteine Levels and All-Cause and Cardiovascular Disease Mortality in Elderly Framingham Men and Women

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