Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

There have recently been increasing experimental and clinical evidences suggesting that hypothalamic dysregulation may be one of the underlying mechanisms of abnormal glucose metabolism. First, increased hypothalamic-pituitary-adrenal axis activity induced by uncontrollable excess stress may cause diabetes mellitus as well as dyslipidemia, visceral obesity, and osteoporosis with some resemblance to Cushing's disease. Second, several molecules are known to be expressed both in pancreas and hypothalamus; adenosine triphosphate-sensitive potassium channels, malonyl-CoA, glucokinase, and AMP-activated protein kinase. Those molecules appear to form an integrated hypothalamic system, which may sense hypothalamic fuel status, especially glucose level, and inhibit action of insulin on hepatic gluconeogenesis, thereby forming a brain-liver circuit. Third, hypothalamic resistance to insulin as an adiposity signal may be involved in pathogenesis of peripheral insulin resistance. The results with mice with a neuron-specific disruption of the insulin receptor gene or those lacking insulin receptor substrate 2 in hypothalamus supported this possibility. Finally, it has very recently been suggested that dysregulation of clock genes in hypothalamus may cause abnormal glucose metabolism. Taken together, it is plausible that some hypothalamic abnormality may underlie at least some portion of type 2 diabetes or insulin resistance in humans, and this viewpoint of hypothalamic pathogenesis of type 2 diabetes may lead to the development of new drugs for type 2 diabetes.
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PMID:Hypothalamic pathogenesis of type 2 diabetes. 1661 35

A new guideline on metabolic syndrome (MS) in Japanese was introduced in 2005. The purpose of this study was to evaluate the prevalence and lifestyle characteristics of Japanese hypertensive patients with MS. Subjects were 290 patients (mean age: 64+/-11 years) who had been followed at our hospital. The waist circumference (WC) and body mass index (BMI) were assessed. Subjects who had BMI >or=25 kg/m(2) were defined as having BMI obesity, while abdominal obesity was defined as a WC >or=85 cm in men and >or=90 cm in women, respectively. Since all patients had hypertension, the definition of MS was made when the patient had abdominal obesity plus either dyslipidemia or glucose intolerance, or both. Among the subjects, 230 patients underwent 24-h home urine collection to measure urinary salt and potassium excretions. Dietary habits were also assessed by use of a questionnaire. Mean values of BMI and WC were 24.2+/-3.4 kg/m(2) and 87.1+/-9.6 cm, respectively. Among the total subject group, 39% patients were classified as having BMI obesity, 49% as having abdominal obesity, and 27% as having MS. BMI was significantly correlated with WC both in men (r=0.86; p<0.01) and in women (r=0.79; p<0.01). More men than women belonged to the BMI obesity (46% vs. 33%, p<0.05), abdominal obesity (63% vs. 39%, p<0.01) and MS (39% vs. 18%, p<0.01) groups. There were no significant differences in blood pressure between patients with and without MS, while patients with MS needed a greater number of antihypertensive drugs than those without MS. Mean urinary salt and potassium excretions were 8.9+/-3.8 g/day and 1.9+/-0.7 g/day, respectively. Urinary salt excretion of <6 g (100 mmol of sodium)/day was achieved in 20% of the subjects. Urinary salt excretion in the patients with MS was significantly higher than that in the patients without (10.1+/-4.2 vs. 8.5+/-3.6 g/day; p<0.01). Only 16% of the patients with MS achieved salt restriction (<6 g/day). The patients with MS had a significantly greater the chance to eat out than the patients without MS. They were also less aware of the need to increase their vegetable consumption. The results suggested that MS is prevalent in Japanese hypertensive patients. Patients with MS showed higher urinary salt excretion and needed more antihypertensive drugs to manage their blood pressure. Dietary counseling focusing not only on sodium restriction but also on the need to increase fruit and vegetable consumption seems to be important.
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PMID:Prevalence and lifestyle characteristics of hypertensive patients with metabolic syndrome followed at an outpatient clinic in fukuoka, Japan. 1825 May 57

According to the "Guideline of the Hypertension Treatment 2004", nutritional recommendation for hypertension is reviewed. The subjects discussed are as follows. 1) restriction of salt (< 6 g/day), 2) advice for vegetables and fruits in connection with potassium and magnesium, 3) control of cholesterol and saturated fatty acid intake, 4) weight control nutritional recommendation for hypertension should be also useful for another atherosclerotic risk factors for example diabetes mellitus, dyslipidemia.
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PMID:[Nutritional recommendation for hypertension]. 1870 May 56

Few population studies have addressed the association of QT interval prolongation with clinical or subclinical arterial disease. The primary objective here was to examine the relationship between the pulse wave velocity (PWV) and the heart rate-corrected QT interval duration (QTc). This is a cross-sectional study, based on a survey of a general population of Japanese. We examined 2,666 community-dwelling individuals without history of cardiovascular disease, aged 40 or over. The PWV was measured between the brachial and ankle regions (baPWV). QTc was estimated using Bazett's equation. The age-adjusted mean values of QTc increased progressively with rising baPWV levels for either sex: for men, 397, 401, 403, and 406 ms for quartile groups defined by baPWV values of less than 1,369, 1,370 to 1,560, 1,561 to 1,840, and 1,841 or greater cm/s, respectively (p < 0.0001 for trend); for women, 406, 410, 414, and 417 ms for quartile groups defined by baPWV of less than 1,269, 1,270 to 1,493, 1,494 to 1,821, and 1,822 or greater cm/s, respectively (p < 0.0001 for trend). When male and female subjects were combined, this positive relationship between baPWV and QTc remained significant, even after controlling for age, sex, hypertension, ECG abnormalities, dyslipidemia, diabetes, obesity, serum calcium and potassium, alcohol intake, and smoking habits (p < 0.0001 for trend). In conclusion, baPWV is independently associated with QT interval prolongation.
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PMID:Arterial stiffness and QT interval prolongation in a general population: the Hisayama study. 1895 4

TREATMENT OF ARTERIAL HYPERTENSION - Blood pressure (BP) should be regularly measured in all patients with CKD (Strength of Recommendation C). - BP control and proteinuria reduction delay progression of CKD (Strength of Recommendation A) and reduce cardiovascular risk (Strength of Recommendation C). Thus, control of both factors should be the treatment objective. - The BP target in patients with CKD should be < 130/80 mmHg, and 125/75 mmHg if proteinuria is > 1 g/24 hours (Strength of Recommendation A). - Lifestyle changes should be made: low-sodium diet (less than 100 mEq/day of sodium or 2.4 g/day of salt); weight reduction if patient is overweight (body mass index 20-25 kg/m2); regular aerobic physical exercise and moderate alcohol intake for BP control and prevention of cardiovascular risk (Strength of Recommendation A). - The choice of the antihypertensive drug in patients with CKD depends on the etiology of CKD, cardiovascular risk, or presence of clinical or subclinical cardiovascular disease (Strength of Recommendation A). - Two or more antihypertensive drugs are usually required to control blood pressure in patients with CKD (Strength of Recommendation B), and will frequently include a diuretic, which in stages 4-5 should be a loop diuretic (Strength of Recommendation B). - Renin-angiotensin-aldosterone system (RAAS) inhibitors are first choice drugs in patients with diabetic nephropathy, patients with non-diabetic nephropathy with a protein/creatinine ratio higher than 200 mg/g, and patients with heart failure (Strength of Recommendation A). The combination of ACEIs and ARBs is indicated for reducing proteinuria that remains high despite treatment with a RAAS inhibitor, provided potassium levels do not exceed 5.5 mEq/L (Strength of Recommendation B). - When RAAS blockers are started or their dose is changed in patients with advanced CKD, kidney function and serum potassium levels should be monitored at least after 1-2 weeks. DIAGNOSIS AND TREATMENT OF DYSLIPIDEMIA - A complete evaluation of the lipid profile including total cholesterol, LDL-C, HDL-C, and triglycerides should be performed in any patient with CKD at baseline and at least annually (Strength of Recommendation B). - In patients with stage 4-5 CKD and LDL-C >or= 100 mg/dL, treatment to decrease levels to < 100 mg/dL should be considered because of their high CV risk. This reduction is recommended in secondary prevention and in primary prevention in diabetic patients. Lipid-lowering treatment is recommended in all other patients, although no evidence showing its benefits is available yet (Strength of Recommendation C). - In patients with stage 4-5 CKD and triglyceride levels >or= 500 mg/dL which are not corrected by treating the underlying cases, treatment with triglyceride-lowering drugs may be considered to reduce the risk of pancreatitis. However, treatment with fibrates should be used with caution, and these drugs should not be associated to statins due to the risk of rhabdomyolysis (Strength of Recommendation C). There is little experience on the efficacy and safety of omega-3 fatty acids for the treatment of hypertriglyceridemia in patients with grade 4-5 CRF, but they may be considered a possibly safer alternative to fibrates (Strength of Recommendation C). SMOKING - Smoking is a cardiovascular risk factor and a risk factor for progression of kidney disease in patients with CRF (Strength of Recommendation B). - Use of active measures to achieve smoking cessation is recommended in patients with CRF (Strength of Recommendation C). HOMOCYSTEINE - Hyperhomocysteinemia has been postulated as a cardiovascular risk factor in the general population and in kidney patients, but the available evidence is not consistent. - There is no evidence that vitamin therapy decreases cardiovascular risk in patients with CRF, and recommendation of routine vitamin measurement and start of vitamin therapy to reduce cardiovascular risk in these patients is therefore questionable (Strength of Recommendation B). LEFT VENTRICULAR HYPERTROPHY - Left ventricular hypertrophy (LVH) is a cardiovascular risk factor in patients with CRF (Strength of Recommendation B). - It is advisable to perform an echocardiogram at baseline and every 12-24 months and to consider treatments allowing for LVH regression (Strength of Recommendation C). The approach to LVH should be early and multifactorial because its reversibility is limited once established (Strength of Recommendation C). - RAAS blockade with ACEIs or ARBs partially reverts LVH in patients with CRF (Strength of Recommendation B). ANTI-PLATELET AGGREGATION - Because of the high cardiovascular risk in patients with CKD, anti-platelet aggregant therapy, especially low-dose aspirin, would be indicated in patients with type 2 diabetes as primary prevention, and in all patients with CKD as secondary prevention. There is however no evidence of the benefits of anti-platelet aggregant therapy in primary prevention in patients with CKD, particularly in stages 4-5; indication for treatment in this situation should therefore be individualised because of its greater risk of bleeding. - Adequate good blood pressure control should previously be achieved to minimise the risk of haemorrhagic stroke (Strength of Recommendation C).
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PMID:[Arterial hypertension and dyslipidemia in patients with chronic kidney disease (CKD). Anti-platelet aggregation. Goal oriented treatment]. 1901 37

Non-immunological factors in the progression of kidney disease in transplant patients are the following: high blood pressure, proteinuria, dislypidemia, etc. 1. Arterial hypertension treatment: Blood pressure must be measured periodically in all transplant patients. Similarly to native kidneys, in renal transplant patients arterial hypertension is a risk factor in the progression of kidney disease. Arterial hypertension represent a clinical marker of chronic allograft nephropathy and contributes to graft loss and to the morbid- mortality of these patients (Evidence level C). Blood pressure control should be < 130/80 mm Hg for renal transplant patients without proteinuria and 125/75 mm Hg for proteinuric patients (> 1 g/24 hours). Hypertension and proteinuria are frequently associated in the same patients, a global treatment of both seems more rational (Evidence level C). General measures should be instigated first with pharmacological therapy. All antihypertensive drugs are useful in renal transplant patients and the majority of patients will need two or more drugs. In proteinuric patients an angiotensin receptor antagonist or an ACE-inhibitor should be initiated. It is advisable to monitor the serum potassium and creatinine after the start of this drugs or during the treatment periodically, especially in patients with chronic kidney disease stage IV-V. 2. Proteinuria treatment: Proteinuria has been strongly correlated with reduced function and graft survival. Lowering proteinuria to values as near to normal as possible (< 0.5 g/24 hours). To reduce proteinuria, an angiotensin receptor antagonist, an ACE-inhibitor or a combination of both are required, with serum potassium or creatinine monitoring, especially in patients with chronic kidney disease stage IV-V. 3. Dyslipidemia treatment: For kidney transplant recipients the assessment of dyslipidemias should include a complete fasting lipid profile with total cholesterol, LDL, HDL, and triglycerides. Evidence from the general population indicates that treatment of dyslipidemias reduces cardiovascular disease and evidence in kidney transplant patients suggests that judicious treatment can be safe and effective in improving dyslipidemia. Therapeutic goal must be LDL < 100 mg/dl. (Evidence level C). 4. Others: Cigarette smoking, glucose intolerance or diabetes control and obesity should be assessed.
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PMID:[Progression factors in chronic kidney disease. Non-immunological mechanisms]. 1967 57

Gallstone disease is one of the major surgical problems in the Libyan population; it is probably related to diet, especially excessive consumption of meat. The study was conducted to determine the composition of gallstones and their possible etiology in a Libyan population. The chemical composition of gallstones from 41 patients (six males and 35 females) was analyzed. The stones were classified into cholesterol, pigment, and mixed stones (MS). Cholesterol stones (CS) showed a significantly higher cholesterol content than pigment stones (PS) (p=0.0085) though not significantly higher than MS. Their phospholipid content and inorganic phosphates were higher than in the other types of stones and oxalate content was significantly elevated in comparison with MS (p=0.0471). In MS, the cholesterol, bile acids, and bilirubin were intermediate between cholesterol and PS, whereas triglycerides were significantly more than PS (p=0.0004). Bilirubin (0.0001) and bile acids (p=0.0009) were significantly higher than CS (p=0.0001). However, they contained the lowest amounts of sodium, potassium, magnesium, and oxalate. In PS, bilirubin (p=0.0001) was significantly higher than both groups. Bile acid content was significantly higher than CS (p=0.0001) but not significantly more than MS. They showed the highest values of calcium, sodium, potassium, magnesium, and chlorides compared to the other types of stones. High levels of cholesterol in stones and dyslipidemia associated with mixed as well as cholesterol gallstones suggest an etiological association and efforts to reduce dietary fat among the Libyan population may lead to decreased cholesterol and mixed gallstones.
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PMID:Quantitative analysis of gallstones in Libyan patients. 2148 49

The prevalence of metabolic syndrome (MetS) manifestations is rapidly increasing worldwide, and is becoming an important health problem. Actually, MetS includes a combination of clinical complications such as obesity (central adiposity), insulin resistance, glucose intolerance, dyslipidemia, non-alcoholic fatty liver disease and hypertension. All these alterations predispose individuals to type 2 diabetes and cardiovascular disease inducing earlier mortality rates among people. In general terms, it is difficult for patients to follow a standard long-term diet/exercise regime that would improve or alleviate MetS symptoms. Thus, the investigation of food components that may deal with the MetS features is an important field for ameliorate and facilitate MetS dietary-based therapies. Currently antioxidants are of great interest due to the described association between obesity, cardiovascular alterations and oxidative stress. On the other hand, high MUFA and PUFA diets are being also considered due to their potential benefits on hypertension, insulin resistance and triglyceride levels. Mineral composition of the diet is also relevant since high potassium intake may improve hypertension and high calcium consumption may promote lipid oxidation. Thus, although nutritional supplements are at the peak of dietetic therapies, the consumption of some specific foods (legumes, fatty fish, vegetables and fruits, etc) with bioactive components within an energy-restricted diet is a promising approach to manage MetS manifestations. Therefore, the present review focuses on some of the most important food components currently investigated to improve and make easier the nutritional MetS treatment.
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PMID:Obesity and metabolic syndrome: potential benefit from specific nutritional components. 2176 73

Magnesium intake of 500 mg/d to 1000 mg/d may reduce blood pressure (BP) as much as 5.6/2.8 mm Hg. However, clinical studies have a wide range of BP reduction, with some showing no change in BP. The combination of increased intake of magnesium and potassium coupled with reduced sodium intake is more effective in reducing BP than single mineral intake and is often as effective as one antihypertensive drug in treating hypertension. Reducing intracellular sodium and calcium while increasing intracellular magnesium and potassium improves BP response. Magnesium also increases the effectiveness of all antihypertensive drug classes. It remains to be conclusively proven that cardiovascular disease such as coronary heart disease, ischemic stroke, and cardiac arrhythmias can be prevented or treated with magnesium intake. Preliminary evidence suggests that insulin sensitivity, hyperglycemia, diabetes mellitus, left ventricular hypertrophy, and dyslipidemia may be improved with increased magnesium intake. Various genetic defects in magnesium transport are associated with hypertension and possibly with cardiovascular disease. Oral magnesium acts as a natural calcium channel blocker, increases nitric oxide, improves endothelial dysfunction, and induces direct and indirect vasodilation.
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PMID:The role of magnesium in hypertension and cardiovascular disease. 2205 30

Dyslipidemia is common in chronic hemodialysis patients and its underlying mechanism is complex. Hemodialysis causes an imbalance between antioxidants and production of reactive oxygen species, which induces the oxidative stress and thereby may lead to accelerated atherosclerosis. Statins have been found to be little effective in end-stage kidney disease and other lipid-lowering therapies have been only scarcely studied. The study aimed to assess the effect of low-dose fenofibrate therapy on plasma lipids and redox status in long-term hemodialysis patients with mild hypertriglyceridemia.Twenty seven chronic hemodialysis patients without any lipid-lowering therapy were included in a double-blind crossover, placebo-controlled study. The patients were randomized into two groups and were given a sequence of either 100 mg of fenofibrate per each hemodialysis day for 4 weeks or placebo with a week-long wash-out period between treatment periods. Plasma lipids, high sensitive C-reactive protein (CRP), urea, creatinine, electrolytes, phosphocreatine kinase (CK), GOT, GPT and plasma thiols (total and free glutathione, homocysteine, cysteine and cysteinylglycine) were measured at baseline and after each of the study periods. Plasma aminothiols were measured by reversed phase HPLC with thiol derivatization with 2-chloro-1-methylquinolinium tetrafluoroborate.Fenofibrate therapy caused a significant decrease of total serum cholesterol, LDL cholesterol and triglycerides and an increase of HDL cholesterol. The treatment was well tolerated with no side-effects but there was a small but significant increase of CK not exceeding the upper limit of normal range. There were no changes of serum CRP, potassium, urea, and creatinine and liver enzymes during the treatment. Neither total nor total free cysteinylglycine and cysteine changed during the study but both total and free glutathione increased during the therapy with fenofibrate and the same was observed in case of plasma homocysteine.The study shows that a treatment with reduced fenofibrate dose is safe and effective in reducing serum triglycerides and cholesterol in chronic dialysis patients and may shift plasma aminothiol balance towards a more antioxidative pattern.
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PMID:Treatment of chronic hemodialysis patients with low-dose fenofibrate effectively reduces plasma lipids and affects plasma redox status. 2256 53


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