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)

In our opinion, this clinical study demonstrates the intravascular formation of globules, macroglobules and their aggregations both in the association with the type of general anaesthesia and with the operative osteosynthesis of long bones. Within the framework of this study changes in the level of lactic acid in blood serum and of total ketosubstances in blood were followed as well as the levels of total lipids, triglycerides, phospholipides, serum lipase, non-esterified and esterified fatty acids, changes in blood coagulation and 17-ketosteroides in blood. The observed changes supported the opinion that the development of fat globulemia was associated with humoral and physicochemical changes in blood. Repeated evaluations of fat globulemia in plasma are important for studies on pathogenesis and development of fat embolism. In practice, they help: to diagnose especially subclinical forms of fat embolism with non-marked clinical symptoms; to define a suitable term of both primary and delayed operation performed in the period of ending katabolic phase after severe trauma; to define an optimum time for the indication of osteosynthesis to the end of manifest fat embolism; to control positive effects of drugs used for the prophylaction and treatment of fat embolism. In this way it is possible to objective the effectiveness of a rational prophylaxis and treatment of fat embolism. Following factors contribute to macroglobulamia and to manifestation of F. E.: injuries to bones, tissues and organs; stress, posttraumatic shock; severe hemorrhagic hypotension; posttraumatic hypercoagulation with possible binding to the development of a consumption coagulopathy; heavy changes of acid-base balance; increase of catecholamines in plasma; hormonal and general metabolic disturbances; posttraumatic dyslipidemia with special regard to the decrease of beta-lipoproteins and of lipoproteinlipase activity together with the increase of lipoproteins having a very low density and with the occurrence of a significant lipoprotein coalescence. The prospective study on the globulemia changes is based on the following examinations: in 76 injured patients: a short time observation (24 hours) of the globulemia changer after osteosyntheses in general anesthesia. The operative interventions were usually performed 6 to 8 days after injury. in 60 injured patients with fractures (single or multiple fractures, fractures in polytrauma patients): a long-time observation (28 days) of the globulemia changes.
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PMID:Fat globulemia in early diagnostics of traumatic fat embolism. 308 41

This paper describes a case of acute pancreatitis occurring in a patient immediately after delivery and in primigravida. The patient had a family case history of dyslipidemia (Type IV). The pregnancy had been complicated by preeclampsia treated at home with nifedipine tablets (one tablet three times a day) with good results on pressure values; lipidic values were high despite dietary measures taken. The baby at birth weighed 3830 g after physiologic labour and a natural delivery. Acute pancreatitis was diagnosed after observation of epigastralgia with irradiation on the left shoulder, vomiting, symptoms of acute abdomen such as sweating, increased pulse rate, hypotension, abdominal pain on palpation, and absence of peristalsis. An analysis of the blood showed high levels of amylase and hyperglycemia, an increase in XDP, and leucocytosis. Instrumental tests such as pancreatic echography revealed an increase in pancreatic volume, uneven structure of the parenchyma and higher levels of liquid in the peritoneum. The patient was moved to intensive-care, a nasal gastric probe inserted, hydroelectrolytic treatment was begun, vital functions monitored, pain kept under control by medical therapy, and antibiotics administered. Subsequent tests showed an improvement in the parameters of pancreatic functions (amylase, lipase, calcium hematic) and their gradual return to normal values. The computerized tomography of abdomen additionally revealed the presence of pancreatic pseudo-cysts and effusion of peritoneal liquid near the right kidney. The patient was discharged after two weeks in the surgical ward. There are many caused of acute abdomen during and immediately after pregnancy, and one of these is acute pancreatitis, though rare (occurring between 1:3800 and 11.467 according to Rabkin).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute pancreatitis in pregnancy]. 835 Oct 66

Chronic renal failure (CRF) is associated with hypertriglyceridemia, impaired clearance of very low density lipoproteins (VLDL) and chylomicrons and their remnants as well as triglyceride-enrichment of various lipoproteins. These abnormalities are indicative of depressed lipoprotein lipase (LPL)-mediated hydrolysis of triglycerides in VLD and chylomicrons. In fact, impaired post-heparin lipolytic activity and decreased adipose tissue LPL activity has been previously demonstrated in CRF. The reduction in LPL activity in CRF has been attributed to PTH-induced insulin resistance and the presence of excess lipase inhibitors in uremic plasma. However, the effect of CRF on gene expression of LPL has not been elucidated and was studied here. Heparin-releasable, detergent-extractable and total LPL activities, as well as LPL mRNA of the heart, soleus muscle and fat body were determined in male Sprague-Dawley rats at baseline and on weeks 1, 3 and 6 following 5/6 nephrectomy (CRF group) or sham operation (control group). The CRF group exhibited a marked and steady rise in plasma triglycerides along with a steady decline in LPL activities and mRNA levels of all tissues studied. In contrast, the study parameters remained virtually unchanged throughout the study period in the control group. A strong inverse correlation was found between plasma triglycerides and LPL activity in the study animals. LPL activity was directly related to LPL mRNA. We conclude that CRF results in marked down-regulation of LPL expression that can contribute to dyslipidemia and altered energy metabolism in uremia. The effect of depressed LPL expression is compounded by the previously demonstrated elevations in uremic plasma of Apo C-III and pre-beta-HDL, which are potent inhibitors of LPL.
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PMID:Down-regulation of tissue lipoprotein lipase expression in experimental chronic renal failure. 894 76

Catecholamines are the only hormones with pronounced lipolytic action in man. A number of in vivo and in vitro studies suggest that there is lipolytic resistance to catecholamines in subcutaneous adipose tissue, which is the major fat depot in obese subjects. This is due to multiple alterations in catecholamine signal transduction, involving decreased expression and function of beta2-adrenoceptors, increased function of alpha2-adrenoceptors and decreased ability of cyclic monophosphate (AMP) to stimulate hormone sensitive lipase. A sedentary life-style, which usually characterizes obesity, may contribute to the catecholamine resistance. However, hereditary/genetic factors may also be involved. Recently, decreased expression and function of hormone sensitive lipase has been found in subcutaneous adipocytes of non-obese subjects with heredity for obesity. In addition, polymorphisms in the genes for beta2-adrenoceptors, beta3-adrenoceptors and hormone sensitive lipase, associate with obesity. On the other hand, catecholamine-induced lipolysis in visceral adipose tissue is increased in obesity due to increased function of beta3-adrenoceptors (major finding), decreased function of alpha2-adrenoceptors and increased ability of cyclic AMP to stimulate lipolysis. When the findings in different adipose regions are considered together, it appears that there is a redistribution of lipolysis and thereby fatty acid mobilization in obesity, favouring the visceral fat depot. This leads to an increase in the circulating fatty acid levels in the portal vein, which connects visceral fat with the liver. As a consequence, the liver function may be altered leading to hyperinsulinemia, hyperglycemia and dyslipidemia, which usually accompany the obese state.
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PMID:Catecholamine-induced lipolysis in obesity. 1019 56

Patients with diabetes mellitus undergoing chronic hemodialysis treatment have the worst outcome on dialysis due to an increased rate of cardiovascular complications. Nearly all patients present with dyslipidemia, a prominent vascular risk factor, probably responsible for the high rate of vascular injury. Since both uremia and diabetes predispose to hypertriglyceridemia, the present study was conducted to investigate the influence of diabetes mellitus and/or hypertriglyceridemia on lipoprotein metabolism in hemodialysis patients. LDL was isolated and characterized from hyper- and normotriglyceridemic diabetic and nondiabetic hemodialysis patients (n = 40; 10 in each group); also, LDL-receptor-dependent uptake and intracellular cholesterol metabolism were studied in HepG2 cells. In addition, scavenger-receptor-mediated uptake was examined in mouse peritoneal macrophages. LDL isolated from nondiabetic normotriglyceridemic hemodialysis patients exhibited impaired cellular uptake via the LDL receptor. Additionally, intracellular sterol synthesis was less inhibited and cholesterol esterification was reduced compared with LDL from healthy control subjects. Reduction of catabolic capacities was more marked in hemodialysis patients who were either diabetic or hypertriglyceridemic and even more pronounced in patients presenting with a combination of both diabetes and hypertriglyceridemia. Hypertriglyceridemic and diabetic patients showed reduced lipase activity and increased LDL oxidation. Furthermore, they accumulated a fraction of small, dense LDL, and LDL was predominantly taken up via the scavenger-receptor pathway in peritoneal macrophages. This study elucidates the distinct influence of diabetes and/or hypertriglyceridemia in hemodialysis patients on cellular LDL metabolism via specific and nonspecific metabolic pathways. Furthermore, it underscores the cumulative impact of these pathologic entities on impairment of lipoprotein metabolism and increase of cardiovascular risk.
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PMID:Non-insulin-dependent diabetes mellitus and hypertriglyceridemia impair lipoprotein metabolism in chronic hemodialysis patients. 1021 33

End-stage renal failure (ESRF) is associated with dyslipidemia and accelerated atherosclerosis. Triglyceride-rich lipoproteins accumulate and qualitative changes take place in low-density lipoprotein (LDL), with a predominance of the small dense LDL phenotype. Increased small dense LDL (LDLIII) is a known risk factor for cardiovascular disease. To assess the extent of LDLIII formation in ESRF and identify factors contributing to LDLIII production, we analyzed LDL subfractions by density-gradient ultracentrifugation, very low-density lipoprotein subfractions, and lipase activity in 75 patients with ESRF (25 hemodialysis [HD], 25 peritoneal dialysis [PD], and 25 predialysis patients) and 40 age- and sex-matched controls. The percentage of LDLIII was increased in all three patient groups compared with controls (PD, 33% +/- 29% [mean +/- SD]; P < 0.005; HD, 30% +/- 22%; P < 0.01; predialysis, 26% +/- 26%; P < 0.01; all versus controls, 14% +/- 10%). Plasma LDLIII concentration was increased only in PD patients (median, 84 mg/dL; interquartile range [IQR], 29 to 160 mg/dL versus controls; median, 31 mg/dL; IQR, 26 to 54 mg/dL). In other patient groups, total LDL level was less, with heterogeneity in LDLIII concentrations. Forty percent of PD patients and 28% of HD and predialysis patients had LDLIII concentrations greater than 100 mg/dL compared with 2.5% of controls (P = 0.002). Plasma triglyceride levels (r(2) = 38.4%; P < 0.001) and hepatic lipase activity (r(2) = 6.7%; P < 0.03) were independent predictors of LDLIII concentration. The strong association between LDLIII concentration and triglyceride level was present in all three patient groups (HD, r(2) = 47.9%; PD, r(2) = 45. 2%; predialysis, r(2) = 25.8%); plasma triglyceride levels greater than 177 mg/dL (2.0 mmol/L) had an 86% specificity and 79% sensitivity for predicting an LDLIII concentration greater than 100 mg/dL. We conclude that the atherogenic lipoprotein phenotype predominates in ESRF, with excess LDLIII particularly prominent in PD patients. Atherogenic levels of LDLIII are found in patients with triglyceride levels greater than 177 mg/dL. This is likely to represent a further cardiovascular risk factor in this population.
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PMID:Atherogenic lipoprotein phenotype in end-stage renal failure: origin and extent of small dense low-density lipoprotein formation. 1079 19

Thyroid hormones influence all major metabolic pathways. Their most obvious and well-known action is an increase in basal energy expenditure obtained acting on protein, carbohydrate and lipid metabolism. With specific regard to lipid metabolism, thyroid hormones affect synthesis, mobilization and degradation of lipids, although degradation is influenced more than synthesis. The main and best-known effects on lipid metabolism include: (a) enhanced utilization of lipid substrates; (b) increase in the synthesis and mobilization of triglycerides stored in adipose tissue; (c) increase in the concentration of non-esterified fatty acids (NEFA); and (d) increase of lipoprotein-lipase activity. While severe hypothyroidism is usually associated with an increased serum concentration of total cholesterol and atherogenic lipoproteins, the occurrence of acute myocardial infarction (AMI) in hypothyroid patients is not frequent. However, hypothyroid patients appear to have an increased incidence of residual myocardial ischemia following AMI. Even in subclinical hypothyroidism, which is characterized by raised serum TSH levels with normal serum thyroid hormone concentrations, mild hyperlipidemia is present and may contribute to an increased risk of atherogenesis. Prudent substitution therapy with L-thyroxine is indicated in patients with both overt and subclinical hypothyroidism, with or without angina, to counteract the cardiovascular risk resulting from hyper-dyslipidemia.
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PMID:Thyroid and lipid metabolism. 1099 23

Postprandial lipemia after an oral fat challenge was studied in middle-aged men with visceral obesity. The two groups had similar plasma cholesterol levels, but obese subjects had higher levels of plasma triglyceride and reduced amounts of high-density cholesterol. Fasting plasma insulin was fourfold greater in obese subjects because of concomitant insulin resistance, with a calculated HOMA score of 3.1 +/- 0.6 vs. 0.8 +/- 0.2, respectively. Plasma apolipoprotein B(48) (apoB(48)) and retinyl palmitate (RP) after an oral fat challenge were used to monitor chylomicron metabolism. Compared with lean subjects, the fasting concentration of apoB(48) was more than twofold greater in obese individuals, suggestive of an accumulation of posthydrolyzed particles. After the oral lipid load, the incremental areas under the apoB(48) and RP curves (IAUC) were both significantly greater in obese subjects (apoB(48): 97 +/- 17 vs. 44 +/- 12 microg.ml(-1). h; RP: 3,120 +/- 511 vs. 1,308 +/- 177 U. ml(-1). h, respectively). A delay in the conversion of chylomicrons to remnants probably contributed to postprandial dyslipidemia in viscerally obese subjects. The triglyceride IAUC was 68% greater in obese subjects (4.7 +/- 0.6 vs. 2.8 +/- 0.8 mM. h, P < 0.06). Moreover, peak postprandial triglyceride was delayed by approximately 2 h in obese subjects. The reduction in triglyceride lipolysis in vivo did not appear to reflect changes in hydrolytic enzyme activities. Postheparin plasma lipase rates were found to be similar for lean and obese subjects. In this study, low-density lipoprotein (LDL) receptor expression on monunuclear cells was used as a surrogate marker of hepatic activity. We found that, in obese subjects, the binding of LDL was reduced by one-half compared with lean controls (70.9 +/- 15.07 vs. 38.9 +/- 4.6 ng LDL bound/microg cell protein, P = 0.02). Because the LDL receptor is involved in the removal of proatherogenic chylomicron remnants, we suggest that the hepatic clearance of these particles might be compromised in insulin-resistant obese subjects. Premature and accelerated atherogenesis in viscerally obese, insulin-resistant subjects may in part reflect delayed clearance of postprandial lipoprotein remnants.
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PMID:Postprandial dyslipidemia in men with visceral obesity: an effect of reduced LDL receptor expression? 1150 Mar 19

Apolipoprotein E (apo E) deficiency (or its abnormalities in humans) is associated with a series of pathological conditions including dyslipidemia, atherosclerosis, Alzheimer's disease, and shorter life span. The purpose of this study was to characterize these conditions in apo E-deficient C57BL/6J mice and relate them to human disorders. Deletion of apo E gene in mice is associated with changes in lipoprotein metabolism [plasma total cholesterol (TC) (>+400%), HDL cholesterol (-80%), HDL/TC, and HDL/LDL ratios (-93% and -96%, respectively), esterification rate in apo B-depleted plasma (+100%), plasma triglyceride (+200%), hepatic HMG-CoA reductase activity (-50%), hepatic cholesterol content (+30%)], decreased plasma homocyst(e)ine and glucose levels, and severe atherosclerosis and cutaneous xanthomatosis. Hepatic and lipoprotein lipase activities, hepatic LDL receptor function, and organ antioxidant capacity remain unchanged. Several histological/immunohistological stainings failed to detect potential markers for neurodegenerative disease in the brain of 37-wk-old male apo E-KO mice. Apo E-KO mice may have normal growth and development, but advanced atherosclerosis and xanthomatosis may indirectly reduce their life span. Apo E plays a crucial role in regulation of lipid metabolism and atherogenesis without affecting lipase activities, endogenous antioxidant capacity, or appearance of neurodegenerative markers in 37-wk-old male mice.
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PMID:Pathophysiology of apolipoprotein E deficiency in mice: relevance to apo E-related disorders in humans. 1172 38

Protease inhibitor-based highly active antiretroviral therapy (PI-HAART) has been implicated in dyslipidemia, peripheral insulin resistance, and abnormal adipose tissue deposition in human immunodeficiency virus (HIV) and acquired immunodeficiency syndrome, or AIDS. In vitro evidence indicates that some PIs reduce adipocyte lipoprotein (LPL) and hepatic lipase (HL) expression and activities. We examined whether LPL and HL activities are reduced in HIV-infected patients with dyslipidemia. Fasting serum lipids, glucoregulatory hormones, and postheparin LPL and HL activities, as well as whole body and regional adiposity, were measured in 19 HIV-seronegative controls, 9 HIV+ patients naive to all anti-HIV medications, 9 HIV+ patients naive to PIs, 9 HIV+ patients with prior PI experience but not currently receiving PIs, and 47 HIV+ patients receiving PI-HAART. The PI-HAART group had low LPL and HL activities. However, multiple linear regression analysis indicated that low postheparin LPL activity contributed only partially to HIV-dyslipidemia. Central adiposity and high C-peptide levels (an indicator of high insulin secretion) were stronger predictors of HIV-dyslipidemia. Low LPL and HL activities, by themselves, were insufficient to explain HIV-dyslipidemia because the PI-naive group had low LPL and HL activities but had normal adiposity, C-peptide levels, and serum lipid and lipoprotein levels. HDL-cholesterol was lower in PI-HAART and PI-naive groups than seronegative controls and was directly associated with LPL activity. These findings suggest that HIV-dyslipidemia is mediated primarily by factors that influence triglyceride and lipoprotein synthesis (e.g., central adiposity and hyperinsulinemia) and mediated only partially by factors that influence triglyceride clearance (e.g., lipase activity).
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PMID:Visceral adiposity, C-peptide levels, and low lipase activities predict HIV-dyslipidemia. 1283 64


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