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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute pancreatitis is a disease characterized by abdominal pain, low-grade fever, abdominal tenderness and rigidity, and moderate elevation of the white blood cell count. A widely used revised classification of pancreatitis is that proposed in 1984 at Marseille. It only distinguishes between acute and chronic pancreatitis. In 61 cases were 40 men and 21 women. The mean age in the total series was 52.5 years. The etiology of the acute condition was alcoholism in 32.8% and biliary tract disease in 23%. In 9.8% the acute pancreatitis is associated with alimentary tract diseases (adipositas, hyperlipidemia). The severity of acute pancreatitis is pathological anatomy determined by three stages. In pathogenesis the process of digestion is caused by activated pancreatic enzyme with acinar cell injury. The acinar cell is normally protected from the action of its own enzymes by elaborate intracellular compartmentation of enzymes. Acute pancreatitis is triggered by pancreatic phospholipase A leading to necrosis of lipolytically active fat cells with release of membrane-toxic fatty acids with following destruction of adjacent tissue. Fat necrosis initiates an acute inflammatory reaction with immigration of granulocytes and liberation of kinins, which activate pancreatic enzyme. Pancreatic enzymes are similar to lysosomal enzymes with regard to substrate specificity. Activation will be also triggered by lysosomal enzymes of necrotic acinar cells.
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PMID:[Acute pancreatitis--etiology, pathological anatomy and pathogenesis]. 226 Mar 61

Proteolytic enzymes, lipase, kinins, and other active peptides liberated from the inflamed pancreas convert inflammation of the pancreas, a single-organ disease of the retroperitoneum, to a multisystem disease. Adult respiratory distress syndrome, in addition to being secondary to microvascular thrombosis, may be the result of active phospholipase A (lecithinase), which digests lecithin, a major component of surfactant. Myocardial depression and shock are suspected to be secondary to vasoactive peptides and a myocardial depressant factor. Coagulation abnormalities may range from scattered intravascular thrombosis to severe disseminated intravascular coagulation. Acute renal failure has been explained on the basis of hypovolemia and hypotension. The renin-angiotensin alterations in acute pancreatitis (AP) as mediators of renal failure need to be studied. Metabolic complications include hypocalcemia, hyperlipemia, hyperglycemia, hypoglycemia, and diabetic ketoacidosis, of which hypocalcemia has been long recognized as an indicator of poor prognosis. The pathogenesis of hypocalcemia is multifactorial and includes calcium-soap formation, hormonal imbalances (e.g., parathyroid hormone, calcitonin, glucagon), binding of calcium by free fatty acid-albumin complexes, and intracellular translocation of calcium. Subcutaneous fat necrosis, arthritis, and Purtscher's retinopathy are rare. The various prognostic criteria of AP and other associated laboratory abnormalities are manifestations of systemic effects. Early recognition and appropriated management of these complications have resulted in improved prognosis of severe AP.
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PMID:Acute pancreatitis: a multisystem disease. 804 85

Platelet-activating factor acetylhydrolase (PAF-AH) is a phospholipase A2 associated with lipoproteins that hydrolyzes platelet-activating factor (PAF) and oxidized phospholipids. We have developed an ELISA for PAF-AH that is more sensitive than previous methods, and have quantified HDL-associated and non-HDL-associated PAF-AH in healthy, hyperlipidemic, and diabetic subjects. In healthy subjects, plasma total PAF-AH concentration was positively correlated with PAF-AH activity and with plasma total cholesterol, triacylglycerol, LDL cholesterol and apolipoprotein B (apoB) concentrations (all P < 0.01). HDL-associated PAF-AH concentration was correlated positively with plasma apoA-I and HDL cholesterol. Subjects with hyperlipidemia (n = 73) and diabetes mellitus (n = 87) had higher HDL-associated PAF-AH concentrations than did controls (P < 0.01). Non-HDL-associated PAF-AH concentration was lower in diabetic subjects than in controls (P < 0.01). Both hyperlipidemic and diabetic subjects had lower ratios of PAF-AH to apoB (P < 0.01) and higher ratios of PAF-AH to apoA-I (P < 0.01) than did controls. Our results show that the distribution of PAF-AH mass between HDLs and LDLs is determined partly by the concentrations of the lipoproteins and partly by the mass of enzyme per lipoprotein particle, which is disturbed in hyperlipidemia and diabetes mellitus.
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PMID:Altered distribution of plasma PAF-AH between HDLs and other lipoproteins in hyperlipidemia and diabetes mellitus. 1286 34

It is a known fact that ethanol increases lipid levels in humans and experimental animals. In this study, we have investigated the effect of dendrodoine analogue (DA), DA-[4-amino-5-benzoyl-2-(4-methoxyphenylamino)-thiazole], on alcohol- and thermally oxidized sunflower oil-induced hyperlipidemia. Ethanol was given to animals at a dose of 5 ml of 20% solution and thermally oxidized sunflower oil at a level of 15% (15 g oil/100 g feed). Our results showed increased activity of aspartate transaminase (AST), alkaline phosphatase (ALP) and gamma-glutamyl transferase (GGT) and increased levels of cholesterol, triglycerides and phospholipids in the plasma of groups given alcohol, thermally oxidized oil and alcohol + thermally oxidized oil when compared with normal control group. The levels of tissue (liver and kidney) cholesterol and triglycerides were increased significantly in groups treated with alcohol, thermally oxidized oil and alcohol + thermally oxidized oil when compared with normal control rats. The levels were decreased when DA was given along with alcohol and thermally oxidized oil. The level of phospholipids decreased significantly in the liver and kidney of rats administered alcohol, thermally oxidized oil and alcohol + thermally oxidized oil when compared with normal control rats. The level increased when DA was administered along with alcohol and thermally oxidized oil. The activity of phospholipase A and C increased significantly in the liver of groups given alcohol, thermally oxidized oil and alcohol + thermally oxidized oil when compared with normal control rats, whereas the activity was decreased upon DA treatment. The obtained results indicate that DA can decrease the lipid levels in alcohol- and thermally oxidized oil-treated rats.
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PMID:Role of an aminothiazole derivative on ethanol- and thermally oxidized sunflower oil-induced toxicity. 1515 74

Ethanol is one of the most widely used and abused drugs, increasing lipid levels in humans and experimental animals. Heating of oil rich in polyunsaturated fatty acids (PUFA) produces various lipid peroxidative end products that can aggravate the pathological changes produced by ethanol. In the present communication, the effect of Cuminum cyminum was investigated on alcohol and thermally oxidized oil induced hyperlipidaemia. The results showed increased activity of aspartate transaminase (AST), alkaline phosphatase (ALP) and gamma glutamyl transferase (GGT) and increased levels of cholesterol, triglycerides and phospholipids in the plasma of rats given alcohol, thermally oxidized oil and alcohol+thermally oxidized oil when compared with the normal control group. The levels of tissue (liver and kidney) cholesterol and triglycerides were increased significantly in rats groups given alcohol, thermally oxidized oil and alcohol+thermally oxidized oil when compared with the normal control rats. The levels were decreased when cumin was given along with alcohol and thermally oxidized oil. The level of phospholipids decreased significantly in the liver and kidney of groups given alcohol, thermally oxidized oil and alcohol+thermally oridized oil when compared with the normal control rats. The level increased when cumin was administered along with alcohol and thermally oxidized oil. The activity of phospholipase A and C increased significantly in the liver of groups given alcohol, thermally oxidized oil and alcohol+thermally oxidized oil when compared with the normal control rats, whereas the activity was decreased with the cumin treatment. The results obtained indicate that cumin can decrease the lipid levels in alcohol and thermally oxidized oil induced hepatotoxicity.
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PMID:Therapeutic role of Cuminum cyminum on ethanol and thermally oxidized sunflower oil induced toxicity. 1610 95

During early pregnancy, long-chain polyunsaturated fatty acids (LC-PUFA) may accumulate in maternal fat depots and become available for placental transfer during late pregnancy, when the fetal growth rate is maximal and fetal requirements for LC-PUFAs are greatly enhanced. During this late part of gestation, enhanced lipolytic activity in adipose tissue contributes to the development of maternal hyperlipidaemia; there is an increase in plasma triacylglycerol concentrations, with smaller rises in phospholipid and cholesterol concentrations. Besides the increase in plasma very-low-density lipoprotein, there is a proportional enrichment of triacylglycerols in both low-density lipoproteins and high-density lipoproteins. These lipoproteins transport LC-PUFA in the maternal circulation. The presence of lipoprotein receptors in the placenta allows their placental uptake, where they are hydrolysed by lipoprotein lipase, phospholipase A(2) and intracellular lipase. The fatty acids that are released can be metabolized and diffuse into the fetal plasma. Although present in smaller proportions, maternal plasma non-esterified fatty acids are also a source of LC-PUFA for the fetus, their placental transfer being facilitated by the presence of a membrane fatty acid-binding protein. There is very little placental transfer of glycerol, whereas the transfer of ketone bodies may become quantitatively important under conditions of maternal hyperketonaemia, such as during fasting, a high-fat diet or diabetes. The demands for cholesterol in the fetus are high, but whereas maternal cholesterol substantially contributes to fetal cholesterol during early pregnancy, fetal cholesterol biosynthesis rather than cholesterol transfer from maternal lipoproteins seems to be the main mechanism for satisfying fetal requirements during late pregnancy.
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PMID:Maternal lipid metabolism and placental lipid transfer. 1661 15

Elevated circulating levels of secretory phospholipase A(2) (sPLA(2)) are associated with atherosclerotic cardiovascular disease. sPLA(2) can contribute to atherogenesis by hydrolyzing phospholipids of circulating lipoproteins and lipoproteins entrapped in the arterial wall and/or in cells that reside in the intima and that participate in the inflammatory response to lipoprotein deposition. This article reviews differences and similarities between sPLA(2)-IIA, sPLA(2)-V, and sPLA(2)-X, all of which are members of this family of enzymes with reported potential proatherogenic features. Published data suggest that each of the enzymes has a distinct profile characterized by differences in tissue expression and localization, capacity to act on phospholipids of cell membranes and lipoproteins, and their interaction with arterial proteoglycans. In addition, the article discusses results from the authors' laboratory showing that diet-induced or gene-induced hyperlipidemia in mice enhances the expression of sPLA(2)-V in different tissues, but not sPLA(2)-IIA. Such differences indicate that these enzymes may have different roles in atherosclerotic cardiovascular disease through their distinct profiles.
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PMID:Role of secretory phospholipases in atherogenesis. 1848 54

Lipid accumulation in arteries induces vascular inflammation and atherosclerosis, the major cause of heart attack and stroke in humans. Extreme hyperlipidemia induced in mice and rabbits enables modeling many aspects of human atherosclerosis, but microscopic examination of plaques is possible only postmortem. Here we report that feeding adult zebrafish (Danio rerio) a high-cholesterol diet (HCD) resulted in hypercholesterolemia, remarkable lipoprotein oxidation, and fatty streak formation in the arteries. Feeding an HCD supplemented with a fluorescent cholesteryl ester to optically transparent fli1:EGFP zebrafish larvae in which endothelial cells express green fluorescent protein (GFP), and using confocal microscopy enabled monitoring vascular lipid accumulation and the endothelial cell layer disorganization and thickening in a live animal. The HCD feeding also increased leakage of a fluorescent dextran from the blood vessels. Administering ezetimibe significantly diminished the HCD-induced endothelial cell layer thickening and improved its barrier function. Feeding HCD to lyz:DsRed2 larvae in which macrophages and granulocytes express DsRed resulted in the accumulation of fluorescent myeloid cells in the vascular wall. Using a fluorogenic substrate for phospholipase A(2) (PLA(2)), we observed an increased vascular PLA(2) activity in live HCD-fed larvae compared to control larvae. Furthermore, by transplanting genetically modified murine cells into HCD-fed larvae, we demonstrated that toll-like receptor-4 was required for efficient in vivo lipid uptake by macrophages. These results suggest that the novel zebrafish model is suitable for studying temporal characteristics of certain inflammatory processes of early atherogenesis and the in vivo function of vascular cells.
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PMID:Vascular lipid accumulation, lipoprotein oxidation, and macrophage lipid uptake in hypercholesterolemic zebrafish. 1926 37

Identification of the widely accepted cardiovascular risk factors of age, sex, hypertension, hyperlipidemia, smoking, obesity, diabetes, and physical inactivity from the Framingham Heart Study have led to dramatic reductions in cardiovascular morbidity and mortality. The Framingham estimation of coronary heart disease remains the mainstay of clinical risk assessment. However, novel risk predictors present opportunities to identify more patients at risk and to more accurately define that risk. Such predictors include lipoprotein analysis, measurement of lipoprotein-associated phospholipase A(2) and C-reactive protein, and assessment of hyperglycemia, liver function, and central obesity. Vascular imaging can also provide useful risk information. Using Framingham as a basis, several international groups have developed risks-coring systems that more closely reflect their individual populations and the clinical practicalities of their countries. When used accordingly, the newer risk predictors build upon the Framingham framework to allow physicians and their patients to effectively minimize, or even avoid, the burden of cardiovascular disease.
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PMID:Updating the assessment of cardiac risk: beyond Framingham. 1959 18

ABSTRACT The protective effect of dendrodoine analog (DA) [4-amino-5-benzoyl-2-(4-methoxy phenylamino) thiazole] at three doses (5, 10, and 15 mg/kg body weight) was investigated on ethanol-induced hyperlipidemia. Hepatotoxicity was induced by administering 7.9 g ethanol/kg body weight for 45 days by intragastric intubation. Our results showed increased activity of aspartate transaminase (AST), alkaline phosphatase (ALP), and gamma glutamyl transferase (GGT) and increased levels of cholesterol, triglycerides, and phospholipids in the plasma of alcohol-given group when compared with normal control group. The levels of tissue (liver and kidney) cholesterol and triglycerides were increased significantly in alcohol control rats when compared with normal control rats. The levels of phospholipids decreased significantly in the liver and kidney of alcohol control rats when compared with normal control rats. The activity of phospholipase A and phospholipase C increased significantly in the liver of alcohol control rats when compared with normal control rats. Intragastric administration of DA at 10 mg/kg body weight effectively lowered the activity of hepatic marker enzymes (GGT, AST, and ALP), phospholipase A, and phospholipase C, and decreased the levels of plasma and tissue lipids. The level of tissue phospholipids increased significantly when DA was administered at a dose of 10 mg/kg body weight along with alcohol when compared with alcohol control group. Thus, we propose that DA exerts a hepatoprotective effect by modulating liver marker enzymes and lipid levels at a dosage of 10 mg/kg body weight.
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PMID:Role of an aminothiazole derivative on ethanol-induced toxicity. 2002 Sep 85


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