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Biomedical subjects

J Selhub

Publications and source records attributed to J Selhub.

169 records · Page 10Linked to original sources
PubMed1971

Synchronization of converging metabolic pathways: activation of the Cystathionine gamma-synthase of Neurospora crassa by methyltetrahydrofolate.

Methyltetrahydrofolate synchronizes the activities of the two branches of the pathway of methionine biosynthesis in Neurospora crassa by serving as an essential activator of cystathionine gamma-synthase and antagonizing the feedback inhibition of this enzyme by S-adenosylmethionine. Activation is specific for the methylated form of folate and increases with increasing glutamate content. The inability of extracts of me-1 and me-6 mutants to form cystathionine that has been previously reported is due to the absence of N(5)-methyltetrahydrofolate from these preparations. Extracts of me-1 mutants lack methyltetrahydrofolate because the organisms are deficient in methylenetetrahydrofolate reductase, and those of me-6 because their methyltetrahydrofolate is quantitatively removed by the procedure employed in the preparation of extracts. The folate of the me-6 organisms differs from that of wild type strains in consisting largely of the monoglutamate rather than higher conjugates.

Biochemical Phenomena↗
PubMedDate not supplied

The relationship of ethanol feeding to the methyl folate trap.

Feeding rats a semiliquid ethanol diet for a period of four weeks produced a hepatic accumulation of the methylating agent N5-methyltetrahydrofolate (N5CH3THF). When the ethanol-containing diet was supplemented with 0.5% betaine, an agent known to promote the generation of methionine and S-adenosylmethionine (SAM) in ethanol-fed animals, the accumulation of N5CH3THF was prevented. One index that the methyl folate trap exists is the hepatic accumulation of N5CH3THF, and a second index is that the N5CH3THF accumulation can be relieved by methionine administration. Since ethanol is shown to produce N5CH3THF accumulation in this study, and since betaine (a generator of methionine and SAM) acts to eliminate this accumulation, it is suggestive that ethanol can contribute to the impairing hepatic condition referred to as the "methyl folate trap."

Alcohol Drinking↗
PubMedDate not supplied

Plasma homocysteine, B vitamins, and amino acid concentrations in cats with cardiomyopathy and arterial thromboembolism.

Arterial thromboembolism (ATE) is a common complication of cats with cardiomyopathy (CM), but little is known about the pathophysiology of ATE. In people, high plasma concentrations of homocysteine and low B vitamin concentrations are risk factors for peripheral vascular disease. In addition, low plasma arginine concentrations have been linked to endothelial dysfunction. The purpose of this study was to compare concentrations of homocysteine, B vitamins, and amino acids in plasma of normal cats to those of cats with CM and ATE. Plasma concentrations of homocysteine, vitamin B6, vitamin B12, folate, and amino acids were measured in 29 healthy cats, 27 cats with CM alone, and 28 cats with both CM and ATE. No differences were found between groups in homocysteine or folate. Mean vitamin B12 concentration (mean +/- standard deviation) was lower in cats with ATE (866 +/- 367 pg/mL) and cats with CM (939 +/- 389 pg/mL) compared with healthy controls (1,650 +/- 700 pg/mL; P < .001). Mean vitamin B6 concentration was lower in cats with ATE (3,247 +/- 1.215 pmol/mL) and cats with CM (3,200 +/- 906 pmol/mL) compared with healthy control animals (4,380 +/- 1,302 pmol/mL; P = .005). Plasma arginine concentrations were lower in cats with ATE (75 +/- 33 nmol/mL) compared with cats with CM (106 +/- 25 nmol/mL) and healthy control animals (96 +/- 25 nmol/ mL; P < .001). Vitamin B12 concentration was significantly correlated with left atrial size. We interpret the results of this study to suggest that vitamin B12 and arginine may play a role in CM and ATE of cats.

Amino Acids↗
PubMedDate not supplied

Family history and premature coronary heart disease.

BACKGROUND: We were interested in studying whether a family history of coronary heart disease (CHD) persisted as a significant risk factor for premature coronary heart disease after adjusting for traditional and nontraditional risk factors. METHODS: Ninety-five case patients with documented premature CHD (occurring in a person less than 60 years old and with greater than 50 percent occlusion of a major epicardial vessel or a documented myocardial infarction) and 95 community-based control patients were examined for risk factors including family history, hypertension, diabetes mellitus, sedentary lifestyle, smoking, body mass index, total cholesterol, high-density lipoprotein cholesterol, triglycerides, low-density lipoprotein cholesterol, lipoprotein(a), homocysteine, and fibrinogen. RESULTS: The risk of premature CHD for a positive family history ranged from an odds ratio (OR) of 3.25 for a standard family history of CHD in a first-degree relative, 5.9 for family history of early CHD in a first-degree relative before the age of 45 years, and 6.1 for a strong family history of CHD defined as CHD in at least two first-degree relatives. Family history persisted as a significant risk factor for premature CHD (OR = 3.9, 95 percent confidence interval [CI] 1.8-8.7) in multiple variable models that included traditional and nontraditional risk factors. It was rare, however, for a person with a positive family history not to have at least two other traditional or nontraditional risk factors. CONCLUSIONS: Family history of CHD should not be considered a simple binary risk factor for premature CHD, and a positive family history of CHD indicates that a person is at high risk for premature CHD independent of traditional and nontraditional risk factors.

Bias↗