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hyperhomocysteinemia/triglyceride
L'enllaç es desa al porta-retalls
Pàgina 1 des de 241 resultats
Hyperhomocysteinaemia, hyperlipidaemia and risk of venous thromboembolism in Shiraz.
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To assess the risk of venous thromboembolism (VTE) associated with hyperhomocysteinaemia (hyper-Hcy) and hyperlipidaemia, we performed a case-control study. Fasting total homocysteine (Hcy), triglyceride and cholesterol levels were assessed in 43 patients with VTE and 43 controls. Mean Hcy level was
Is hyperhomocysteinemia an additional risk factor of the metabolic syndrome?
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The aim of this study was to ascertain if hyperhomocysteinemia is associated with the metabolic syndrome. The metabolic syndrome is a cluster of cardiovascular risk factors. Hyperhomocysteinemia is an obvious independent risk factor for atheroma, and thrombosis morbidity and mortality. EPIMIL is a
Allicin improves carotid artery intima-media thickness in coronary artery disease patients with hyperhomocysteinemia.
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Homocysteine (Hcy) is an important and independent risk factor for atherosclerotic diseases, such as coronary artery disease and ischemic cerebrovascular disease. Increased carotid artery intima-media thickness (IMT) is a non-invasive marker of systemic atherosclerosis. Allicin treatment may
Hyperhomocysteinemia, lipid and lipoprotein disturbances in patients with primary hypertension.
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OBJECTIVE
The main aim of the study was to answer two questions: what are the concentrations of total cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides, apo A-I (apolipoprotein A-I), apo B (apolipoprotein B) and Lp(a) (lipoprotein(a)) in serum of patients with primary hypertension and
Cysteinemia, rather than homocysteinemia, is associated with plasma apolipoprotein A-I levels in hyperhomocysteinemia: lipid metabolism in cystathionine beta-synthase deficiency.
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OBJECTIVE
Genetic and dietary hyperhomocysteinemia has been found to decrease high density lipoproteins (HDL) and their apolipoprotein A1 (APOA1). To test the hypothesis that the presence of cysteine could normalize HDL levels in hyperhomocysteinemic cystathionine beta-synthase (Cbs)-deficient mice
Factors contributing to the resistivity of a higher casein diet against choline deficiency-induced hyperhomocysteinemia in rats.
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The mechanism by which feeding a higher casein diet results in resistance to choline deprivation-induced hyperhomocysteinemia was investigated in rats. Plasma homocysteine concentration was significantly lower in rats fed a 30% casein diet (30C) than in rats fed a 10% casein diet (10C). Choline
Hyperhomocysteinemia and related factors in 600 hospitalized elderly subjects.
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Hyperhomocysteinemia (HHcy) is a metabolic disorder frequently occurring in the elderly population. Recently several reports have suggested abnormalities in homocysteine (tHcy) metabolism implicating HHcy as a metabolic link in the multifactorial processes characterizing many geriatric
Hyperhomocysteinemia and hypercholesterolemia associated with hypothyroidism in the third US National Health and Nutrition Examination Survey.
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Hypothyroid (thyroid stimulating hormone (TSH)> or =20 mIU/l; N=32) participants in the third National Health and Nutrition Examination Survey, Phase 2 (1991-1994) were compared with non-hypothyroid subjects (0.5 mIU/l
Omega-3 PUFA ameliorates hyperhomocysteinemia-induced hepatic steatosis in mice by inhibiting hepatic ceramide synthesis.
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Hyperhomocysteinemia (HHcy) is a key risk factor in hepatic steatosis. In this study, we applied a metabolomic approach to investigate the changes in the metabolite profile due to HHcy-induced hepatic steatosis and the effects of omega-3 PUFA (polyunsaturated fatty acid) supplementation in mice.
Nuclear factor erythroid 2-related factor 2 activation mediates hyperhomocysteinemia-associated lipolysis suppression in adipocytes.
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Hyperhomocysteinemia (HHcy) is associated with suppressed lipolytic response in adipocytes/adipose tissue, however, the underlying mechanism remains to be extensively studied. Nuclear factor erythroid 2-related factor 2 (Nrf2), a master transcriptional factor regulating antioxidant generation, has
[Prevalence of hyperhomocysteinemia and related factors in a community-based health examination survey: a cross-sectional study].
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BACKGROUND
Many previous studies have shown that elevated homocysteine in the serum is a well known risk factor for cardiovascular disease and this is associated with other risk factors for cardiovascular disease, but any Korean data on this is limited.
OBJECTIVE
This study aimed to calculate the
Effect of alcohol consumption on risk of hyperhomocysteinemia based on alcohol-related facial flushing response.
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BACKGROUND
This study examined the relationship between alcohol consumption and hyperhomocysteinemia based on facial flushing caused by drinking.
METHODS
Among male patients aged ≥ 18 years who visited Health Promotion Center of Chungnam National University Hospital in Daejeon from January 2008 to
Abnormal lipid metabolism in cystathionine beta-synthase-deficient mice, an animal model for hyperhomocysteinemia.
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Hyperhomocysteinemia (HHCY) is a consequence of impaired methionine/cysteine metabolism and is caused by deficiency of vitamins and/or enzymes such as cystathionine beta-synthase (CBS). Although HHCY is an important and independent risk factor for cardiovascular diseases that are commonly associated
Hyperhomocysteinemia, enzyme polymorphism and thiobarbituric Acid reactive system in children with high coronary risk family history.
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OBJECTIVE
To investigate both the frequency and the genetic background of hyperhomocysteinemia and the frequency of increased plasma thiobarbituric acid reactive system (TBARS) levels in children and adolescents whose parents had premature coronary heart disease (CHD).
METHODS
The study was
[Treatment of hyperhomocysteinemia and endothelial dysfunction in renal-transplant recipients with vitamin B].
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OBJECTIVE
To study the effect of vitamin B on treatment of hyperhomocysteinemia and endothelial dysfunction in renal-transplant recipients.
METHODS
Thirty-six stable hyperhomocysteinemic renal-transplant recipients were randomly assigned to vitamin treatment (group A, n = 18, folic acid 5 mg/d,
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