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)

Most epidemiological surveys on risk factors of atherosclerosis were cross-sectional in design and did not consider the existence of pathologically distinct processes. The Bruneck Study is a prospective survey in the general community (age range, 40 to 79 years). The baseline examination and first reevaluation were performed in the summers of 1990 and 1995 (participation, 92%; follow-up, 96%). Carotid atherosclerosis was monitored with high-resolution duplex ultrasound. Early (incidence and/or extension of nonstenotic lesions) and advanced (incidence and/or progression of stenosis >40%) stages of atherogenesis were differentiated. The risk profile of early atherogenesis consists of traditional risk factors, such as hypertension, hyperlipidemia, and cigarette smoking (pack-years), supplemented by a variety of less well-established risk conditions, including high body iron stores, hypothyroidism, microalbuminuria, and high alcohol consumption. In contrast, the risk profile of advanced atherogenesis includes markers of enhanced prothrombotic capacity, attenuated fibrinolysis, and clinical conditions known to interfere with coagulation: high fibrinogen, low antithrombin, factor V Leiden mutation, lipoprotein(a) >0.32 g/L, high platelet count, cigarette smoking, and diabetes. Hyperlipidemia and hypertension were of only minor relevance. These findings, along with the epidemiological features of advanced atherogenesis and emergence of an elevated fibrin turnover, suggest atherothrombosis to be a key mechanism in the development of advanced stenotic atherosclerosis. Supplementary 6-category logistic regression models illustrate the changing association between major risk predictors and atherosclerosis of increasing severity and substantiate appropriateness of the 40% threshold applied for the definition of advanced stenotic atherosclerosis. Atherosclerosis is a heterogeneous process that subsumes etiologically and epidemiologically distinct disease entities. The multifactorial etiology of atherosclerosis, which goes far beyond the traditional risk factors, has not yet achieved adequate attention in clinical practice and disease prevention.
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PMID:Distinct risk profiles of early and advanced atherosclerosis: prospective results from the Bruneck Study. 1066 53

Iron deficiency anemia and hyperlipidemia are common public health problems in Turkey. The connection between iron and lipid metabolisms has not been clarified yet. The aim of the study was to determine the effect of iron deficiency on carnitine and lipid metabolism. Study group was consisted of 70 children (mean age 14.7 +/- 1.3 months) suffering from iron deficiency anemia and 20 healthy children (mean age 13.7 +/- 1.2 months) attended to outpatient clinics of Cumhuriyet University, Sivas were enrolled the study as the control group. Assessments of serum free carnitine concentrations, total triglyceride, total cholesterol and VLDL levels were made in both groups. The mean serum free carnitine concentration was significantly lower than the control group (18.9 +/- 0.43 nmol/ml and 45.9 +/- 1.47 nmol/ml respectively, t = 17.5 p < 0.01). Results of our study also indicated higher serum total triglyceride, total cholesterol and VLDL levels in iron deficient patients than the healthy controls. Regression analyses indicated a negative correlation between serum free carnitine and total triglyceride levels in iron deficient patients. This study confirms that iron deficiency anemia may be linked to the endogenous carnitine synthesis in pediatric age group, and thus hyperlipidemia appears to be a risk factor for premature cardiovascular diseases.
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PMID:Serum free carnitine and total triglycerid levels in children with iron deficiency anemia. 1127 25

Disturbances in lipid metabolism during copper deficiency in rats are well recognized. Copper deficiency is associated with the spontaneous retention of hepatic iron. Previous studies have reported that hypercholesterolemia and hypertriglyceridemia are associated with elevated hepatic iron concentrations in copper deficient rats. There was a direct relationship between the magnitude of blood lipids and the concentration of hepatic iron. Based on these data, it has been hypothesized that iron was responsible for the development of lipemia of copper deficiency. In this study was determined the effect of increasing doses of Cu(10, 20 and 50 ppm) in the diet, on the serum total lipids, total cholesterol, triglycerides (triacylglicerols), phospholipids, non-esterified fatty acids (NEFA) and liver iron and zinc concentrations in normal rats. The results were compared with normal rats that received a balanced diet containing 0.6 and 6 ppm of Cu, respectively. The results show that Cu-supplement diminished the cholesterol and triglyceride serum levels, increased the level of phospholipids, NEFA and concomitantly decreased the hepatic concentrations of Fe and Zn. There was a statistically significant (p < 0.05) simple correlation between triglycerides and liver Fe (r = 0.917; R2 = 64.03%), cholesterol and liver Zn (r = 0.872; R2 = 76.07%), cholesterol and liver Fe (r = 0.995; R2 = 99.10%), liver Fe and liver Cu (r = -0.612), liver Fe and liver Zn (r = 0.837), liver Cu and liver Zn (r = -0.612), and serum triglycerides and liver Zn (r = 0.967). The mechanism(s) by which Fe and Zn determine these changes is not known; none of the enzymes that act in cholesterol and triglyceride metabolism and biosynthesis require Fe and/or Zn. The increase of NEFA is due to changes in the process of lipolysis and re-esterification of the fatty acids in blood. However, additional studies are needed for the precise mechanisms of this interrelationships to be clarified.
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PMID:[Changes in serum lipids in rats treated with oral cooper]. 1134 94

In the past year there have been many advances in the area of small bowel physiology and pathology and therapy. In preparation for this review, over 1500 papers were assessed. The focus is on presenting clinically useful information for the practising gastroenterologist. Selected important clinical learning points include the following: (1) glucose absorption mediated by SGLT1 is controlled by mRNA abundance, as well as by posttranscriptional processes including protein trafficking; (2) inducers of cytochrome P-450 decrease glucose and fructose absorption and increase glucose consumption in the intestine; (3) the regulated release of nutrients from the stomach into the upper intestine ensures that the modest intestinal transport reserve capacity is not exceeded; (4) hepatocyte growth factor and short-chain fatty acids may enhance intestinal adaptation and prevent the atrophy seen when total parenteral nutrition is infused; (5) inhibitors of pancreatic lipase and phospholipase H2 may be useful clinically to reduce absorption as part of a treatment program for obesity and hyperlipidemia; (6) several membrane-bound and cytosolic proteins have been identified in the enterocyte as well as in the hepatocyte and may be the target for the future therapeutic manipulation of bile acid metabolism and control of hyperlipidemia; (7) suspect bile acid malabsorption in the patient with otherwise unexplained chronic diarrhea; (8) a proportion of lipid absorption is protein-mediated, and this opens the way to targeting these proteins and thereby therapeutically modifying lipid absorption; (9) a high protein diet may be useful to increase the intestinal absorption of drugs transported by the H+/dipeptide cotransporter; (10) a metal transporter DCT1 has been identified, and this may open the way to a better understanding of disorders of, for example, iron and zinc metabolism; (11) the nutrient transporters such as SGLT1 are responsible for a portion of the intestinal absorption of water; (12) the influence of nitric oxide on intestinal water absorption and secretion depends on its concentration; (13) a trial of bile acid-sequestering agent may prove useful in the treatment of the patient who experiences diarrhea while taking an enteral diet; (14) a proteolytic extract from pineapple stems may prove to be useful to treat diarrhea, although the mechanism of this effect remains to be established; and (15) the antisecretory effect of the new peptide, sorbin, needs to be tested in a clinical situation on patients with diarrhea. Other new and promising antidiarrheal agents include bromelain, an extract from pineapple stems, and igmesine, a final sigma ligand.
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PMID:Small bowel review: normal physiology part 1. 1176 47

This article describes the first autopsy case of heme oxygenase (HO)-1 deficiency. A 6-year-old boy who presented with growth retardation; anemia; leukocytosis; thrombocytosis; coagulation abnormality; elevated levels of haptoglobin, ferritin, and heme in serum; a low serum bilirubin concentration; and hyperlipidemia was diagnosed as HO-1 deficient by gene analysis several months before death. Autopsy showed amyloid deposits in the liver and adrenal glands and mesangioproliferative glomerular changes in kidneys, in addition to an irregular distribution of foamy macrophages with iron pigments. Fatty streaks and fibrous plaques were noted in the aorta. Compared with HO-1--targeted mice, the present case seems to more severely involve endothelial cells and the reticuloendothelial system, resulting in intravascular hemolysis, disseminated intravascular coagulation, and amyloidosis with a short survival. This contrasts to the predominant iron metabolic disorders of HO-1--targeted mice with a long survival.
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PMID:Heme oxygenase-1 deficiency: the first autopsy case. 1182 83

Patients with end-stage renal disease (ESRD) are at a markedly increased risk for cardiovascular complications compared with the general population. In addition to traditional cardiovascular risk factors such as diabetes mellitus, hypertension, hyperlipidaemia or cigarette smoking, a number of population-specific factors are implicated, such as anaemia, hyperhomocysteinaemia, hyperphosphataemia and vascular calcification, as well as inflammation and oxidative stress. Iron overload has been suggested to increase the cardiovascular risk in the general population. Iron supplementation is a widespread clinical practice in ESRD, especially in patients on maintenance haemodialysis (HD). Iron may therefore contribute to cardiovascular complications through effects on low-density lipoprotein oxidation and endothelial dysfunction. Although the effects of iron stores and iron therapy on cardiovascular risk are not well defined in HD patients, the 'iron hypothesis' deserves attention: serum ferritin is a marker of morbidity and mortality in HD patients, and the administration of high amounts of intravenous iron increases the risks of hospitalization and death. In contrast to intravenous iron therapy, intestinal iron absorption is regulated by body iron stores and is suppressed in the presence of infection and iron overload. Prospective studies are needed to clarify the influence of iron stores and iron therapy on overall and cardiovascular morbidity and mortality in ESRD patients.
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PMID:Iron overload and cardiovascular complications in dialysis patients. 1190 55

Stearoyl-CoA desaturase (SCD) is a short-lived, polytopic membrane-bound non-heme iron enzyme localized primarily in the endoplasmic reticulum. SCD is required for the biosynthesis of monounsaturated fatty acids, and plays a key role in hepatic synthesis of triglycerides and very-low-density lipoproteins. The intracellular concentration of SCD fluctuates in a wide range in response to complex and often competing hormonal and dietary factors. A combination of transcriptional regulation and rapid protein degradation produces transient elevations of SCD enzyme activity in response to physiologic demands. Dysregulation of SCD has been implicated in non-alcoholic fatty liver disease, hyperlipidemia, and obesity.
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PMID:Stearoyl-CoA desaturase, a short-lived protein of endoplasmic reticulum with multiple control mechanisms. 1253 76

It was hypothesized that subjects with metabolic syndrome (hypertension, obesity, hyperlipidemia, diabetes mellitus): (1) develop measurable peripheral edema at moderate altitude and (2) might show differences on erythropoiesis, iron status and vascular endothelial growth factor (VEGF) in comparison to healthy subjects during and after a long-term stay (3-week exposure) at moderate altitude (congruent with 1700 m). Twenty-two male subjects with metabolic syndrome were selected. Baseline investigations (t1) were performed in Innsbruck (500 m). All participants were transferred by bus to 1700 m (Alps) and remained there for 3 weeks with examinations on day 1 (after the first night at altitude, t2), day 4 (t3), day 9 (t4) and day 19 (t5). After returning to Innsbruck, post-altitude examinations were conducted after 7-10 days (t6) and 6-7 weeks (t7), respectively. Body mass was decreased from t1 to t7 (P<0.01). Total body water was decreased at t2 (P<0.01), returned to control level (t3, t4), and was found elevated at t7 (P<0.01). Lean body mass did not change, but body fat decreased during the study (P<0.01). Tissue thickness at the forehead decreased during and after altitude exposure (P<0.01), whereas tissue thickness at the tibia did not alter. Erythropoietin (EPO) was elevated as early as t2 and remained increased until t5. Reticulocyte count was increased at t3 and remained above pre-altitude values. VEGF levels were unchanged. After a 3-week exposure to moderate altitude, patients with metabolic syndrome had reduced their body mass, mainly because of a reduction in body fat. The moderate altitude was found to stimulate erythropoiesis in these patients but this was not sufficient to increase serum VEGF concentration.
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PMID:Austrian Moderate Altitude Study (AMAS 2000) - fluid shifts, erythropoiesis, and angiogenesis in patients with metabolic syndrome at moderate altitude (congruent with 1700 m). 1256 Sep 47

Our understanding of nutrient absorption continues to grow, from the development of unique animal models and from studies in which cutting-edge molecular and cellular biologic approaches have been used to analyze the structure and function of relevant molecules. Studies of the molecular genetics of inherited disorders have also provided many new insights into these processes. A major advance in lipid absorption has been the cloning and characterization of several intestinal acyl CoA:monoacylglycerol acyltransferases; these may provide new targets for antiobesity drug therapy. Studies of intestinal cholesterol absorption and reverse cholesterol transport have encouraged the development of novel potential treatments for hyperlipidemia. Observations in genetically modified mice and in humans with mutations in glucose transporter 2 suggest the importance of a separate microsomal membrane transport pathway for glucose transport. The study of iron metabolism has advanced greatly with the identification of the hemochromatosis gene and the continued examination of the genetic regulation of iron absorptive pathways. Several human thiamine transporters have been identified, and their specific roles in different tissues are being explored.
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PMID:Nutrient absorption. 1570 23

Hepatic steatosis is the hallmark of nonalcoholic fatty liver disease (NAFLD), which is the consequence of multiple metabolic derangements among which insulin resistance plays a pivotal role. Steatosis is, also, a feature of hepatitis C virus (HCV) infection. However, in chronic hepatitis C, the prevalence of steatosis is 2.5-fold more elevated than that expected by a chance concurrence with NAFLD, suggesting that HCV may be implied in the development of steatosis. As observed in NAFLD, in patients infected with HCV genotype 1 steatosis is associated with an increased body mass index. On the other hand, in patients infected with genotype 3 the extent of steatosis strictly correlates with the viral load indicating that steatosis is mainly "virus-related". Regardless of the "metabolic" or "viral" etiology, hepatic steatosis in HCV contributes to the progression of liver fibrosis, to the development of hepatocellular carcinoma and to an impaired response to interferon treatment. Features such as obesity, insulin resistance and type 2 diabetes mellitus are shared by NAFLD and HCV-associated steatosis. In addition, HCV infection, directly or through steatosis, favors the development of type 2 diabetes mellitus. Hyperlipidemia is an independent predictor of the development of NAFLD, but not of HCV-associated steatosis. Arterial hypertension is common in nonalcoholic steatohepatitis patients, and HCV infection has recently been acknowledged as an independent risk factor for atherosclerosis. The role of iron in the progression of both NAFLD and HCV-associated steatosis remains controversial while lipoperoxidation and oxidative stress are pathogenic mechanisms shared by both. Some metabolic risk factors may be shared by both HCV-associated steatosis and NAFLD although the disease progression and pathophysiological background may be different. Preliminary data suggest that the therapeutic options for NAFLD may also be useful to improve HCV-associated steatosis.
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PMID:[Hepatitis C virus-associated and metabolic steatosis. Different or overlapping diseases?]. 1585 90


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