Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interrelations between hypertension (HT), ischemic heart disease (IHD) and diabetes mellitus (DM) were investigated in the diabetic subjects without IHD (DM group) or with IHD (DM + IHD group) and subjects with IHD (IHD group) which were not complicated with DM. 1. The incidence of hypertension of DM group, DM+IHD group and IHD group is 40, 54, 38% respectively. 2. The incidence of hyperlipidemia of DM group, DM + IHD group and IHD group is 55, 71, 56% respectively. 3. Serum Mg levels of DM (1.9 +/- 0.37 mg/dl), DM + IHD (1.8 +/- 0.23) and IHD (1.9 +/- 0.33) were significantly lower than that of normal control (2.3 +/- 0.32). 4. Serum Mg level of poorly controlled diabetic patients is lower than that of well controlled diabetic patients. These results suggested that Magnesium deficient state is one of the cause of insulin resistancy.
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PMID:Hypertension and serum Mg in the patients with diabetes and coronary heart disease. 924 Jul 68

Glucose stabilizes the mRNA for human fatty acid synthase (FAS), an enzyme relevant to diverse human disorders, including hyperlipidemia, obesity, and malignancy. To determine the underlying mechanisms, RNA gel mobility shift assays were used to demonstrate that human Hep G2 cells contain a cytoplasmic factor that binds specifically to the 3'-terminus of the human FAS mRNA. D-Glucose increased RNA-binding activity by 2.02-fold (P = 0.0033), with activity peaking 3 h after glucose feeding. Boiling or treatment of extracts with proteinase K abolished binding. Ultraviolet cross-linking of the FAS mRNA-binding factor followed by SDS-PAGE resolved a proteinase K-sensitive band with an apparent molecular mass of 178 +/- 7 kDa. The protein was purified to homogeneity using nondenaturing polyacrylamide gels as an affinity matrix. Acid phosphatase treatment of the protein prevented binding to the FAS mRNA, but binding activity was unaffected by modification of sulfhydryl groups and was not Mg2+ or Ca2+ dependent. Deletion and RNase T1 mapping localized the binding site of the protein to 37 nucleotides characterized by the repetitive motif ACCCC and found within the first 65 bases of the 3'-UTR. Hybridization of the FAS transcript with an oligonucleotide antisense to this sequence abolished binding. These findings indicate that a 178-kDa glucose-inducible phosphoprotein binds to an (ACCCC)n-containing sequence in the 3'-UTR of the FAS mRNA within the same time frame that glucose stabilizes the FAS message. This protein may participate in the posttranscriptional control of FAS gene expression.
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PMID:Properties and purification of a glucose-inducible human fatty acid synthase mRNA-binding protein. 957 16

Ageing constitutes a risk factor for magnesium deficit. Primary magnesium deficit originates from two etiological mechanisms: deficiency and depletion. Primary magnesium deficiency is due to insufficient magnesium intake. Dietary amounts of magnesium are marginal in the whole population whatever the age. Nutritional deficiencies are more pronounced in institutionalized than in free-living ageing groups. Primary magnesium depletion is due to dysregulation of factors controlling magnesium status: intestinal magnesium hypoabsorption, reduced magnesium bone uptake and mobilisation, sometimes urinary leakage, hyperadrenoglucocorticism by decreased adaptability to stress, insulin-resistance and adrenergic hyporeceptivity. Secondary magnesium deficit in ageing largely results from various pathologies and treatments common to elderly persons: i.e. non insulin dependent diabetes mellitus and use of hypermagnesuric diuretics. Magnesium deficit may participate in the clinical pattern of ageing: mainly neuromuscular, cardiovascular and renal symptomatologies. The consequences of hyperadrenoglucocorticism--whose non response to dexamethasone suppression test appears the simplest marker--may concern immunosuppression, muscle atrophy, centralization of fat mass, osteoporosis, hyperglycemia, hyperlipidemia, atherosclerosis, disturbances in mood and mental performances through accelerated hippocampal ageing particularly. Treatment of magnesium deficiency requires simple oral physiological magnesium supplementation. Treatment of the different types of magnesium depletion leads to a more or less specific control of pathophysiological disturbances of the required magnesium substrate. Open and double blind studies on the effects of the treatments of magnesium deficiency and of magnesium depletions in geriatic populations are too scarce. Further study is necessary to assess the accurate place of magnesium deficit in the physiopathology of ageing.
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PMID:Magnesium status and ageing: an update. 959 47

Advanced arterial wall calcification in atherosclerosis imposes a serious rupturing effect on the aorta. However, the mechanism of dystrophic calcification linked to hyperlipidemia, that causes atherosclerosis remains unknown. Emerging morphological and biochemical evidence reveals that calcifiable vesicles may have a role in plaque calcification. To determine whether a high cholesterol diet can induce arterial calcification and produce or activate calcifiable vesicles in aortas, a rabbit model was used. After 2 months of daily high lipid feeding (supplemented with 2% cholesterol and 6% peanut oil), typical atherosclerotic lesions developed. However, the mineral, if present in aortas, was insufficient to be detected by Fourier transform-infrared spectroscopy (FT-IR) or alizarin red staining, indicative of a non-calcifying stage of atherosclerosis. Small segments of thoracic aortas were digested in a crude collagenase solution to release calcifiable vesicles. Vesicles were also isolated from normal aortas as control to consider the possibility that membrane vesicles may be produced by crude collagenase digestion, which could cause the degradation of some cells. Calcifiable vesicles were precipitated at 300,000 x g after subcellular particles were removed by centrifugation at 30,000 x g. Calcifiability of isolated vesicles was then tested using calcifying media containing physiological levels of Ca2+ and Pi and 1 mM ATP. Electron microscopic observations showed that the isolated vesicles were heterogeneous in size and shape and capable of depositing electron dense particles. Fourier transform infrared spectroscopic analysis of the deposited particles revealed the presence of an amorphous mineral phase. The spectroscopic mineral to matrix ratios, related to the amount of mineralization, indicated that vesicles from cholesterol-fed rabbits produced more minerals than control vesicles obtained from the normal aortas. Alizarin red staining for mineral further demonstrated substantially higher calcifiability of the experimental vesicles. A 3-5 h exposure of the vesicles to calcifying media caused significant deposition of 45Ca and 32Pi in a vesicle protein-concentration dependent manner. Similar to previously reported observations with human atherosclerotic aorta vesicles, rabbit vesicles were enriched in ATP-hydrolyzing enzymes including Mg2+- or Ca2+-ATPase and NTP pyrophosphohydrolase that are implicated in normal and pathological calcification. Altogether, these observations suggest that accumulation of the released calcifiable vesicles, as a result of high cholesterol diets, may have a role in dystrophic calcification in hyperlipidemia-related atherosclerosis.
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PMID:Isolation of calcifiable vesicles from aortas of rabbits fed with high cholesterol diets. 1116 22

Magnesium is the fourth most abundant cation in the body and is present in more than 300 enzymatic systems, where it is crucial for adenosine triphosphate (ATP) metabolism. Deficiency states result in increased insulin resistance, as well as increased smooth muscle and platelet reactivity. Magnesium deficiency has been shown to correlate with a number of chronic cardiovascular diseases, including hypertension, diabetes mellitus, and hyperlipidemia. Intravenous magnesium has been used therapeutically in critical situations such as status asthmaticus, torsades de pointes, and preeclampsia. Few controlled studies exist regarding the therapeutic uses of oral magnesium supplementation in chronic cardiovascular diseases. Randomized clinical trials are urgently needed to determine whether magnesium supplementation will alter the natural history of these disease states.
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PMID:Magnesium: its proven and potential clinical significance. 1260 35

According to the Vital Statistics Report published by the Japanese Ministry of Health and Welfare, heart disease and cerebrovascular disease are the main causes of death in Japan. The main pathological finding in these diseases is atherosclerosis and the main risk factors, besides the patient's age and diathesis, include hyperlipidemia, hypertension, diabetes, obesity and smoking. Among the aforementioned various risk factors, hyperlipidemia play a crucial role at the stage of atherosclerosis. The main pathological findings in atherosclerosis include abnormal reactions of neutrophils, lymphocytes and monocytes/macrophages, vascular smooth muscle cells and vascular endothelial cells, and the accumulation of cholesterol ester in the arterial wall. Previously, Mg(2+) deficit and the lower blood concentration of Mg(2+) was a frequent in patients with the main risk factors, hyperlipidemia, hypertension, diabetes, and obesity. Magnesium is necessary the activity of lecithin cholesterol acyltransferase (LCAT) and lipoprotein lipase (LPL), which lowers triglyceride levels and raises HDL-cholesterol levels. Moreover, Mg(2+)-ATP is also the controlling factor for the rate-limiting enzyme in the cholesterol biosynthesis, which associated with cholesterol levels. In this article, we first discuss the effect of Mg(2+) deficit on atherosclerosis, especially hyperlipidemia in bloodstream and liver. Then, based on recent studies including our own, we describe the Mg(2+) deficit and the relationships between risk factors for atherosclerosis, hypertension, oxidative stress, cholesterol reverse transport system, and the molecular mechanisms, especially peroxisome preoliferator-activated receptor (PPAR), which have the pleiotropic effect in atherosclerosis. The mechanism is likely the effect of Mg(2+) on atherosclerosis.
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PMID:[Lipid metabolism and magnesium]. 1627 15

Magnesium (Mg) plays an essential role in a wide range of fundamental cellular reactions in patients with ischemic heart disease. It has been well known that Mg plays a pivotal role in control of cardiac excitability, neuromuscular transmission, vasomotor tone, and blood pressure, among other functions. Especially, many epidemiological, experimental, and clinical studies support a pathological role for Mg in the etiology and development of major coronary risk factors as diabetes mellitus, hypertension, and hyperlipidemia as well as ischemic heart disease. Furthermore, the therapeutic value of Mg in the management of coronary risk factors and ischemic heart disease has been clarified. Dietary Mg supplementation should be considered as a preventive element in atherosclerosis and ischemic heart disease.
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PMID:Magnesium and ischemic heart disease: a review of epidemiological, experimental, and clinical evidences. 1654 43

We developed a simple separative method for measuring serum amyloid A (SAA) in both high-density-lipoprotein (HDL) and low-density-lipoprotein (LDL) fractions. It was devised using the SAA agglutination method and phosphotungstic acid-Mg2+ precipitation procedure for evaluating HDL-cholesterol (HDL-C). The new method is also able to detect amyloid A (AA) in each fraction with precision. The results of both the present method and the method using SAA agglutination and the dextran sulfate-Mg2+ precipitation procedure showed a strong correlation when used to measure the level of SAA in the LDL fraction of patients (r = 0.997; p < 0.0001). Reference intervals in normal healthy subjects (n=75) ranged from 0.5 to 4.7 microg/ml in the HDL fraction and from 0.1 to 1.9 microg/ml in the LDL fraction. SAA in the LDL fraction of subjects with hyperlipidemia was significantly higher than in normal subjects and subjects with normal lipidemia. SAA in the HDL fraction and total sera of subjects with hyperlipidemia was significantly higher than in normal subjects; however, it was not higher than in patients with normal lipidemia. The present methods for detecting SAA, especially in the LDL fraction, might benefit from analyzing patho-physiological events in various lipid disorders.
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PMID:[A simple separative method for measuring serum amyloid A in high-density-lipoprotein and low-density-lipoprotein fractions using the phosphotungstic acid-Mg2+ precipitation procedure]. 1751 Dec 61

Magnesium is the fourth most abundant cation in the body and is involved in over 302 enzymatic reactions. Basic science research has implicated magnesium deficiency as a cause of insulin resistance which is related to hypertension, diabetes, hyperlipidemia and increased cardiovascular risk. Research in magnesium deficiency states has been hindered because magnesium is an intracellular ion and difficult to measure. Our goal was to develop a reproducible assay to measure intracellular magnesium in platelets. Healthy volunteers agreed to have blood drawn for magnesium measurement. Platelet rich plasma was harvested from a venipuncture specimen and run through the flow cytometer. A standard titer curve using known increasing concentrations of magnesium chloride was created for each specimen, and then with the other half the specimen was run to measure the true intracellular free magnesium concentration. 15 adults agreed to volunteer for this experiment. All standard titer curves for all specimens had a correlation of > 0.99. The mean concentration of intracellular free magnesium was 450.05 microM with a range of 203.68 microM to 673.50 microM. Intracellular free magnesium can reliably and reproducibly be measured in platelets using Mag Green fluorescent dye and flow cytometry. This should advance our ability to study magnesium deficient states.
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PMID:A method for measuring intracellular free magnesium concentration in platelets using flow cytometry. 1797 63

The scientific literature provides extensive evidence of widespread magnesium deficiency and the potential need for magnesium repletion in diverse medical conditions. Magnesium is an essential element required as a cofactor for over 300 enzymatic reactions and is thus necessary for the biochemical functioning of numerous metabolic pathways. Inadequate magnesium status may impair biochemical processes dependent on sufficiency of this element. Emerging evidence confirms that nearly two-thirds of the population in the western world is not achieving the recommended daily allowance for magnesium, a deficiency problem contributing to various health conditions. This review assesses available medical and scientific literature on health issues related to magnesium. A traditional integrated review format was utilized for this study. Level I evidence supports the use of magnesium in the prevention and treatment of many common health conditions including migraine headache, metabolic syndrome, diabetes, hyperlipidemia, asthma, premenstrual syndrome, preeclampsia, and various cardiac arrhythmias. Magnesium may also be considered for prevention of renal calculi and cataract formation, as an adjunct or treatment for depression, and as a therapeutic intervention for many other health-related disorders. In clinical practice, optimizing magnesium status through diet and supplementation appears to be a safe, useful, and well-documented therapy for several medical conditions.
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PMID:The Importance of Magnesium in Clinical Healthcare. 2909 83


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