Folate-mediated incorporation of ring-2-carbon of histidine into nucleic acids: Influence of thyroid hormone

Nair, C. P. P.; Viswanathan, Gomathy; Noronha, J. M.

doi:10.1016/0026-0495(94)90019-1

Cited by 38 publications

(18 citation statements)

References 13 publications

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“…The apparent close relation between the plasma homocysteine and thyroid hormone levels indicates a hormone effect on homocysteine metabolism, distribution, or clearence. A similar argument can be made for the creatinine and cholesterol responses [8][9][10][11][12][13][14].…”

Section: Discussionmentioning

confidence: 67%

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Plasma Homocysteine Levels in Hyperthyroid Patients

et al. 2004

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Abstract. Hyperhomocysteinemia is a risk factor for premature atherosclerotic vascular diseases. It is known that plasma homocysteine levels are higher in hypothyroid patients compared to healthy subjects. The aim of our study was to assess plasma total homocysteine concentrations in hyperthyroid patients before and after treatment when euthyroid status was reached and compare them with control group. Thirteen hyperthyroid patients (age, 42.9 ± 15.6 year) and eleven healthy subjects (age, 39.9 ± 12.5 year) were involved in the study. Plasma levels of homocysteine and serum cholesterol, triglyceride, HDL cholesterol, urea, creatinine, vitamin B12, folate were measured before and after treatment. LDL cholesterol and creatinine clearences were calculated. Pretreatment homocycteine levels of the hyperthyroid patients were significantly lower than healthy controls (11.5 ± 3.6 mmol/L vs. 15.1 ± 4.5 mmol/L, respectively, p<0.05). Posttreatment homocysteine levels were significantly higher than pretreatment levels (13.9 ± 6.3 mmol/L vs. 11.5 ± 3.6 mmol/L, respectively, p<0.05) and posttreatment creatinine clearance were lower than pretreatment level (103.5 ± 12.7 ml/min vs. 114.2 ± 9.3 ml/min, respectively, p<0.01). Lower homocysteine levels in hyperthyroidism can be partially explained with the changes in creatinine clearance.

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Section: Discussionmentioning

confidence: 67%

“…Folate response was related to direct effect of thyroid hormones on folate metabolizing enzymes, including methylenetetrahydrofolate reductase [8,10,18]. Barbe et al found lower serum folate in the hypothyroid compared with the hyperthyroid state, and they observed the usual inverse relationship between serum folate an homocysteine [7,19].…”

Section: Discussionmentioning

confidence: 99%

Plasma Homocysteine Levels in Hyperthyroid Patients

et al. 2004

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“…Secondly, impaired liver metabolism of Hcy linked with hypothyroidism may contribute to hyperhomocysteinemia. Decreased activity of both enzymes, methionine synthase and methylenetetrahydrofolate reductase was established in thyroidectomized rats and may also explain the elevated level of Hcy in hypothyroidism [15][16][17].…”

Section: Introductionmentioning

confidence: 99%

Serum homocysteine levels are decreased in levothyroxine-treated women with autoimmune thyroiditis

Owecki

Dorszewska

Sawicka‐Gutaj

et al. 2014

EJEA

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Background: Hyperhomocysteinemia is a well-known cardiovascular risk factor and its elevation is established in overt hypothyroidism. Since some authors suggest that chronic autoimmune thyroiditis per se may be considered as a novel risk factor of atherosclerosis independent of thyroid function, the analysis of classical cardiovascular risk factors might be helpful in evaluation the causative relationship. Data concerning the impact of thyroid autoimmunity in euthyroid state on homocysteine (Hcy) level is lacking. The aim of this study was to evaluate Hcy level in context of anti-thyroperoxidase antibodies (TPOAbs) in euthyroidism. Methods: It is a case-control study. 31 euthyroid women treated with levothyroxine (L-T4) due to Hashimoto thyroiditis (HT) and 26 females in euthyroidism without L-T4 replacement therapy were enrolled in the study. All women with HT had positive TPOAbs. Forty healthy females negative for TPOAbs comparable for age and body mass index (BMI) participated in the study as controls. Exclusion criteria were a history of any acute or chronic disease, use of any medications (including oral contraceptives and vitamin supplements), smoking, alcoholism. Results: TPOAbs titers were higher in both groups of HT patients versus the healthy controls. Hcy levels were found to be significantly lower in treated HT patients (Me 11 μmol; IQR 4.2 μmol) as compared with healthy controls (Me 13.35 μmol; IQR 6.34 μmol; p = 0.0179). In contrast, no significant difference was found between non treated HT and control group in Hcy level. The study groups and the controls did not differ in age and BMI. Furthermore, levels of TSH, FT4, TC, LDL, HDL and TAG did not differ between the study group and the control group. Conclusion: The main finding of the study is a decrease in Hcy level in treated HT as compared with healthy controls. Based on our observations one can also assume that correct L-T4 replacement was associated here with a decrease of Hcy. Furthermore, it seems that non treated HT in euthyroidism is not associated with Hcy increase, in contrast to overt hypothyroidism. This may be just another argument against the concepts about the role of "euthyroid HT" in the development of atherosclerosis.

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“…Thyroid hormone was shown to modulate the expression of genes involved in the metabolism of homocysteine and reduce serum homocysteine levels 48,49) . However, changes in folate levels 50) or renal function 51) were reported to be the major determinants of the increased serum homocysteine level in patients with hypothyroidism.…”

Section: Direct Effects Of Thyroid Hormone On the Vasculaturementioning

confidence: 99%

Thyroid Hormone and Vascular Remodeling

Ichiki

2016

JAT

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Both hyperthyroidism and hypothyroidism affect the cardiovascular system. Hypothyroidism is known to be associated with enhanced atherosclerosis and ischemic heart diseases. The accelerated atherosclerosis in the hypothyroid state has been traditionally ascribed to atherogenic lipid profile, diastolic hypertension, and impaired endothelial function. However, recent studies indicate that thyroid hormone has direct anti-atherosclerotic effects, such as production of nitric oxide and suppression of smooth muscle cell proliferation. These data suggest that thyroid hormone inhibits atherogenesis through direct effects on the vasculature as well as modification of risk factors for atherosclerosis. This review summarizes the basic and clinical studies on the role of thyroid hormone in vascular remodeling. The possible application of thyroid hormone mimetics to the therapy of hypercholesterolemia and atherosclerosis is also discussed.

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Folate-mediated incorporation of ring-2-carbon of histidine into nucleic acids: Influence of thyroid hormone

Cited by 38 publications

References 13 publications

Plasma Homocysteine Levels in Hyperthyroid Patients

Plasma Homocysteine Levels in Hyperthyroid Patients

Serum homocysteine levels are decreased in levothyroxine-treated women with autoimmune thyroiditis

Thyroid Hormone and Vascular Remodeling

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