Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study aims at determining serum nitrite/nitrate (NO(x)) levels in healthy subjects within the framework of a population-based study. NO(x) concentration was measured in 3505 subjects aged > or =20 years. Subjects with diabetes, renal dysfunction, those undergoing treatment for dyslipidemia and hypertension, were excluded; also excluded were smokers, pregnant women, and subjects with cardiovascular and infectious diseases or cancer; leaving 1983 (667 men, 1316 women) asymptomatic non-smoking subjects for the analysis. NO(x) concentrations were determined in serum and compared in different age groups. Mean+/-SE of NO(x) concentration was 24.8+/-0.02 and 24.4+/-0.01 micromol/l in men and women respectively. Men aged 20-29 years had significantly higher NO(x) levels compared to corresponding women (25.1+/-0.03 vs. 22.7+/-0.02). Serum NO(x) concentration peaked at 50-59 years in both genders. Comparison between lower and upper quartiles of NO(x) levels was performed in both genders. Women with high serum NO(x) were older and had significantly higher body mass index and fasting plasma glucose. The results of this study determine the normal levels of serum NO(x) concentrations in asymptomatic non-smoker subjects; also show that serum NO(x) concentrations indicate sex and age differences in these subjects.
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PMID:Serum nitric oxide metabolite levels in a general healthy population: relation to sex and age. 1866 5

Prostate cancer, the most frequent non-cutaneous malignancy in aging men, is a growing medical problem, representing the second leading cause of male cancer deaths. Despite its high morbidity, the etiology of prostate cancer remains largely unknown. Several studies have documented hormonal imbalance, such as alteration in androgens and estrogens, obesity, family history and growth factors, as risk factors in the pathogenesis of prostate cancer. Insulin is a growth-promoting hormone that is reported to be involved in the pathogenesis of various malignancies, such as breast and bladder cancers. Insulin is known to increase cancer risk through its effect on cell proliferation, differentiation and apoptosis. In the last decade, converging evidence from epidemiological and clinical studies suggests that the insulin is involved in the tumorigenesis and neoplastic growth of the prostate. Several mechanisms have been suggested to explain the possible causal relationship between insulin and prostate cancer, such as the sympathoexcitatory effect of insulin, alteration of sex hormone metabolism, insulin-like growth factor pathway, signal transduction mechanism and dyslipidemia. The present paper reviews relevant existing studies related to the role of insulin in the pathogenesis of prostate carcinoma.
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PMID:Insulin: a novel agent in the pathogenesis of prostate cancer. 1866 51

Determining the type of cardiac dysfunction is important for implementing therapeutic strategies and for prognostic insights. We characterized systolic dysfunction (SD) and isolated diastolic dysfunction (IDD) in adults referred for echocardiographic evaluation, and compared their clinical and other characteristics. In the present work, we studied 218 patients (137 males) with cardiac dysfunction (mean age, 66.3 +/- 8.3 years). SD was defined as a left ventricular ejection fraction (LVEF) of < 45%, whereas IDD was defined as a LVEF >or= 45% in addition to the standard Doppler-echocardiography diagnostic criteria for IDD. Approximately 68% of subjects had SD (70% males). The proportions of hypertension, diabetes, and dyslipidemia were 44%, 26%, and 22%, respectively, without significant association with the type of dysfunction. Myocardial infarction (MI) was found in 31% of patients, and was significantly (P < 0.001) more prevalent among SD compared with IDD cases. Cerebral stroke (18%) and malignancy (16%) were significantly associated with IDD (29% versus 13% for SD in the case of stroke, and 26% versus 11% for SD in the case of malignancy; P = 0.008 for each). In multivariately-adjusted logistic regression analysis, the following variables were found to be significantly (P < 0.05) and independently associated with IDD: female gender (odds ratio [OR] = 2.207 [95% CI = 1.302-4.608]), stroke (OR = 2.009 [1.119-3.980]), and malignancy (OR = 2.016 [1.230-4.010]). On the other hand, previous MI (OR = 2.075 [1.769-4.808]) was independently associated with SD. In conclusion, some factors/comorbidities were more likely to associate with IDD (female gender, stroke, and malignancy) or SD (previous MI) when IDD and SD were compared with each other.
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PMID:Comparative analysis of systolic and isolated diastolic dysfunction: Sado heart failure study. 1875 29

Systemic fungal infections are increasingly reported in immunocompromised patients with hematological malignancies, recipients of bone marrow and solid organ allografts, and patients with AIDS. Mycoses may infiltrate endocrine organs and adversely affect their function or produce metabolic complications, such as hypopituitarism, hyperthyroidism or hypothyroidism, pancreatitis, hypoadrenalism, hypogonadism, hypernatremia or hyponatremia, and hypercalcemia. Antifungal agents used for prophylaxis and/or treatment of mycoses also have adverse endocrine and metabolic effects, including hypoadrenalism, hypogonadism, hypoglycemia, dyslipidemia, hypernatremia, hypocalcemia, hyperphosphatemia, hyperkalemia or hypokalemia, and hypomagnesemia. Herein, we review how mycoses and conventional systemic antifungal treatment can affect the endocrine system and cause metabolic abnormalities. If clinicians are equipped with better knowledge of the endocrine and metabolic complications of fungal infections and antifungal therapy, they can more readily recognize them and favorably affect outcome.
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PMID:Endocrine and metabolic manifestations of invasive fungal infections and systemic antifungal treatment. 1877 5

Radiation therapy is a cause of cardiovascular morbidity and mortality. This is due to the significant degree of atherosclerosis seen in the vessels in the vicinity of the area being irradiated. Radiation-induced peripheral arterial disease is increasingly being recognized as large populations of cancer patients survive longer, yet it is a problem that is often under reported. Although it has most commonly been associated with carotid artery disease, all vascular beds are prone to this form of injury. The injury is accelerated by usual risk factors for atherosclerosis. Developing a healthy lifestyle, dietary prudence and the aggressive treatment of hypertension, diabetes mellitus, and dyslipidemia should all be encouraged in this patient population. When revascularization strategies are warranted, the percutaneous approach may be superior to open surgery as technical difficulties may arise in the fibrotic, scarred tissue. Stenting with distal embolic protection devices should be considered as the treatment of choice for patients with radiation-induced carotid artery disease. Several reports also suggest good results with balloon angioplasty with or without stenting in the case of radiation-induced renal, iliac, and femoral artery disease. Lifelong antiplatelet therapy may be appropriate.
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PMID:Radiation-induced peripheral artery disease. 1881 53

We investigate whether preadmission hyperglycemia is a risk factor for developing in-hospital symptomatic pulmonary embolism after major orthopedic surgery. Medical records of patients undergoing total hip or total knee arthroplasty from January 2001 to April 2006 were reviewed. The incidence of PE was 1.47% (107/7282 patients). Multivariate analysis showed that preadmission blood glucose (BG) of at least 200 mg/dL independently increased the risk of pulmonary embolism by 3.19 times (P = .015), when compared with patients with BG of less than 110 mg/dL. Other significant risks factors were age (>or=70 years old), body mass index of more than 30 kg/m(2), and congestive heart failure. Total knee had 2.19 times (P = .002) more risk than total hip arthroplasty and bilateral procedure increased the risk by 2.13 times (P = .015). Sex, American Society of Anesthesiologists status, duration of surgery, malignancy, pulmonary disease, hypertension, diabetes mellitus, dyslipidemia, sleep apnea, and stroke were not found to be significant risk factors for pulmonary embolism.
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PMID:Preadmission hyperglycemia is an independent risk factor for in-hospital symptomatic pulmonary embolism after major orthopedic surgery. 1905 17

The aim of present study was to identify the visceral adipose tissue genes differentially expressed in a well-characterized rat model of high-fat diet (HFD)-induced obesity. Male Sprague-Dawley rats were fed either the HFD (17 g lard + 3 g corn oil/100 g) or the normal diet (5 g corn oil/100 g) for 9 weeks. The HFD rats weighed 55% more and accumulated 85% to 133% greater visceral fats than did the normal-diet rats (P < .05). Animals given the HFD for 9 weeks acquired dyslipidemia, fatty liver, insulin resistance, and hyperleptinemia along with the overexpression of several obesity-related genes, such as leptin, tumor necrosis factor alpha, resistin, peroxisome proliferator-activated receptor gamma2, CCAAT/enhancer-binding protein alpha, and sterol regulatory element-binding protein-1c, in the epididymal adipose tissue. The differential gene expression profile obtained from the cDNA microarray analysis followed by the real-time polymerase chain reaction confirmation led to a recruitment of several uncharacterized adipose tissue genes responding to the HFD. We report herein, for the first time, that a series of genes which might be implicated in the insulin-stimulated glucose transporter 4 translocation, such as protein phosphatase 2 (formerly 2A), cell division cycle 42-interacting protein 4, syntaxin 6, linker of T-cell receptor pathways 10, as well as the genes which might be involved in cancer development, such as heat shock 10-kd protein 1, and ras-related C3 botulinum toxin substrate 1, were differentially expressed in the epididymal adipose tissue of rats rendered obese by an HFD.
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PMID:Genes are differentially expressed in the epididymal fat of rats rendered obese by a high-fat diet. 1908 40

Polyunsaturated fatty acids (PUFAs) are essential structural components of all cell membranes and, more so, of the central nervous system. Several studies revealed that n-3 PUFAs possess anti-inflammatory actions and are useful in the treatment of dyslipidemia. These actions explain the beneficial actions of n-3 PUFAs in the management of cardiovascular diseases, inflammatory conditions, neuronal dysfunction, and cancer. But, the exact molecular targets of these beneficial actions of n-3 PUFAs are not known. Mice engineered to carry a fat-1 gene from Caenorhabditis elegans add a double bond into an unsaturated fatty acid hydrocarbon chain and convert n-6 to n-3 fatty acids. This results in an abundance of n-3 eicosapentaenoic acid and docosapentaenoic acid specifically in the brain and a reduction in n-6 fatty acids of these mice that can be used to evaluate the actions of n-3 PUFAs. Gene expression profile, RT-PCR and protein microarray studies in the hippocampus and whole brain of wild-type and fat-1 transgenic mice revealed that genes and proteins concerned with inflammation, apoptosis, neurotransmission, and neuronal growth and synapse formation are specifically modulated in fat-1 mice. These results may explain as to why n-3 PUFAs are of benefit in the prevention and treatment of diseases such as Alzheimer's disease, schizophrenia and other diseases associated with neuronal dysfunction, low-grade systemic inflammatory conditions, and bronchial asthma. Based on these data, it is evident that n-3 PUFAs act to modulate specific genes and formation of their protein products and thus, bring about their various beneficial actions.
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PMID:Gene and protein expression profiling of the fat-1 mouse brain. 1913 87

Lipid-lowering drugs are one of the most prescribed drugs worldwide. The aim was to compare 10-year all-cause mortality according to initial dyslipidemia status and lipid-lowering drug exposure. The PRIME study was a multicenter population-based prospective cohort study of men recruited in 1991 to 1993, aged 50 to 59 years at baseline, and followed up for 10 years. The 4 groups compared were normolipidemic, untreated dyslipidemic, and dyslipidemic subjects on fibrate or statin therapy. Data were analyzed using multivariate Cox models. The cohort included 7,722 French men (statin group 4.0%, fibrate group 7.9%, untreated dyslipidemic subjects 19.0%, and normolipidemic subjects 69.1%). After 10 years, 4.8% of the sample was lost to follow-up and 416 deaths occurred (cancers 53.1%, cardiovascular diseases 17.1%, and other 29.8%). After adjustment for center, age, educational level, cardiovascular risk factors, lipids, alcohol intake, and history of cardiovascular and severe chronic diseases, hazard ratios (HRs) for all-cause mortality were 0.49 (95% confidence interval [CI] 0.26 to 0.94, p = 0.031) for subjects treated with a statin, 0.65 (95% CI 0.42 to 0.99, p = 0.046) for those on fibrate therapy, and 0.76 (95% CI 0.56 to 1.03, p = 0.080) for normolipidemic men compared with untreated dyslipidemic subjects. In the statin group, HRs for death from cardiovascular disease, cancer, and other causes were 0.55 (p = 0.348), 0.41 (p = 0.067), and 0.68 (p = 0.546) compared with dyslipidemic subjects, respectively. In the fibrate group, HRs were 0.76 (p = 0.499), 0.52 (p = 0.041), and 0.87 (p = 0.746). In conclusion, in this cohort study carried out in a real-life setting, all-cause mortality was significantly lower in dyslipidemic subjects on fibrate or statin therapy than in untreated dyslipidemic patients. No excess risk of noncardiovascular death was observed.
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PMID:Ten-year all-cause mortality in presumably healthy subjects on lipid-lowering drugs (from the Prospective Epidemiological Study of Myocardial Infarction [PRIME] prospective cohort). 1916 93

High-density lipoprotein cholesterol (HDL-C) has been suggested to be associated with breast cancer. However, the roles of HDL-C and hypertriglyceridemia on breast cancer still have been controversial. The goal of this study was to investigate the association between HDL-C with breast cancer risk, stratifying by menopausal status, and body mass index. The hormonal receptor status of breast has been proposed to modify the effect of HDL-C on breast cancer. Multicenter hospital-based case-control study was conducted from November 2004 to December 2005 in Korea. After one to two individual matchings by age (+/-5 years) and menopausal status, 690 cases and 1,380 controls were included in the analysis. Odds ratios (OR) and 95% confidence intervals (95% CI) were estimated by conditional, unconditional, and multinomial logistic regressions. Protective effect of HDL-C on breast cancer was only observed among premenopausal women with an OR (95% CI) of 0.49 (0.33-0.72) for HDL-C > or = 60 versus <50 mg/dL (P(trend) < 0.01). Only nonobese premenopausal women had a significant decreased risk (OR, 0.34; 95% CI, 0.22-0.53). OR (95% CI) of low HDL-C (<50 mg/dL) and high triglyceride (TG; > or = 150 mg/dL) category was 2.20 (1.32-3.67) on estrogen receptor-negative and progesterone receptor-negative breast cancer compared with high HDL-C (> or = 50 mg/dL) and low TG (<150 mg/dL) category. This study suggests that higher level of HDL-C may reduce breast cancer risk among premenopausal women. Estrogen receptor-negative and progesterone receptor-negative breast cancer was associated with dyslipidemia, which implicates that association among HDL-C, TG, and breast cancer may be modified by receptor status.
Cancer Epidemiol Biomarkers Prev 2009 Feb
PMID:Serum high-density lipoprotein cholesterol and breast cancer risk by menopausal status, body mass index, and hormonal receptor in Korea. 1919 Jan 59


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