Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of fish oil dietary supplementation on the dyslipidemia and coagulopathy of seven patients with nephrotic syndrome and hypoalbuminemia due to primary kidney disease was studied. Plasma lipids, platelet aggregation studies, simplate bleeding time, and fibrinogen levels were determined before and after 6 wk of treatment with fish oil (15 g/day of MaxEPA; 2.7 g of eicosapentenoic acid (EPA) and 1.8 g of docosahexenoic acid. Urea kinetics were determined from urine-urea concentration, urinary proteina, and urine volume. A 3-day dietary intake record was obtained from each patient before and after 6 wk of fish oil supplementation. There was no significant dietary change in protein, fat, or carbohydrate intake over the time period of the study. At study end, total triglycerides decreased from 2.98 +/- 1.31 to 2.18 +/- 1.14 mmol/L (P = 0.002), and very low-density lipoprotein-triglycerides decreased from 2.35 +/- 1.34 to 1.28 +/- 1.07 mmol/L (P = 0.01). Low-density lipoprotein (LDL) cholesterol increased from 5.18 +/- 1.74 to 7.35 +/- 2.83 mmol/L (P = 0.005). No significant changes occurred in bleeding time, platelet count, hematocrit, red blood cell flexibility, or whole blood viscosity. Platelet aggregation responses to collagen and arachidonic acid were consistently reduced after treatment, but there was no change in platelet response to ADP. The platelet membrane phospolipids showed a significantly increased incorporation of EPA after the fish oil diet (P = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Omega-3 fatty acid supplementation in primary nephrotic syndrome: effects on plasma lipids and coagulopathy. 147 28

Insulin resistance is associated not only with the classic cardiovascular risk factors of hypertension and dyslipidemia, but also with several disorders of coagulation and fibrinolysis. Elevated concentrations of the fibrinolytic inhibitor plasminogen activator inhibitor-1 are associated with insulin resistance. In experimental systems, increased expression and secretion of plasminogen activator inhibitor-1 by hepatocyte and endothelial cell lines can be induced by insulin, proinsulin-like molecules, triglyceride-rich lipoproteins and oxidized LDL, as well as by inducing insulin resistance in isolated hepatocytes. Concentrations of the endothelial cell protein von Willebrand factor are elevated in insulin-resistant states, suggesting that abnormalities of capillary endothelium, as well as those reported for endothelium-dependent vasodilatation, may play a role in the etiology of insulin resistance. Levels of a third coagulation factor, fibrinogen, are elevated in insulin-resistant subjects, an association that suggests a possible role for acute-phase cytokines in the abnormalities of coagulation and endothelial function. It is proposed that the recent observations of secretion of interleukin-6 by adipose tissue, combined with the actions of adipose tissue-expressed tumor necrosis factor-alpha in obesity-induced insulin resistance, could underlie the associations of insulin resistance with endothelial dysfunction, coagulopathy, and coronary heart disease.
 ...
PMID:Abnormalities of coagulation and fibrinolysis in insulin resistance. Evidence for a common antecedent? 1018 59

There is considerable evidence that insulin and insulin-like growth factors regulate a number of important physiological functions in a variety of tissues, some not considered to be classically insulin sensitive. Impaired biological responses to insulin and related insulin-like growth factors are referred to as insulin resistance. Persons with insulin resistance often display clinical abnormalities other than impaired glucose tolerance, including central obesity, hypertension, dyslipidemia, microalbuminuria, and abnormal coagulation and fibrinolytic systems. The mechanisms leading to development of insulin resistance are not fully understood. However, in addition to abnormalities of phosphorylation processes, it appears that alterations in cellular cation metabolism contribute to diminished cellular actions of insulin (i.e., glucose transport and hemodynamic actions). This review focuses on known cellular cation abnormalities and associated insulin resistance and cardiovascular disease.
 ...
PMID:Insulin, cation metabolism and insulin resistance. 1021 36

Growth hormone (GH) deficiency in adults is characterized by central obesity, dyslipidemia, coagulopathy and glucose intolerance, all features of the "metabolic syndrome", explaining the increased cardiovascular morbidity and mortality associated with GH deficiency in adults. Employing the 2-step euglycemic-hyperinsulinemic clamp, we have demonstrated severe insulin resistance in GH-deficient adults, with a reduction in insulin-mediated glucose utilization of -50%. Basal glucose turnover and partitioning of whole body glucose utilization into glycolytic flux (GF) and glycogen synthesis/glucose storage (GS) pathways are normal, but insulin activation of these 2 pathways is reduced, predominantly in the GS pathway. Activation of muscle glycogen synthase by insulin is markedly decreased, as is glycogen content of muscle. Insulin-induced muscle hexokinase activity appears also to be attenuated in GH-deficient adults with raised intramuscular cellular glucose and normal-reduced concentrations of glucose-6-phosphate. Beta-cell function is not excessive in GH-deficient adults and is inappropriately low for the insulin resistance. Following treatment of GH-deficient adults with recombinant GH (rhGH), the insulin resistance is either unchanged or more pronounced by 3, 6 or 24 months of treatment, despite the significant reduction in general and central obesity. The GF and GS pathways and muscle glycogen synthase and hexokinase activities remain severely impaired. Abnormalities in free fatty acid (FFA) metabolism are present in rhGH-treated GH-deficient adults and correlate significantly with the degree of insulin resistance as do the concentrations of rhGH-induced insulin-like growth factor (IGF)-I, the post-basal insulinemia and the duration of the GHD, but is independent of obesity. In conclusion, long-term rhGH treatment in GH-deficient adults results in persistent insulin resistance and abnormalities in the GF and GS pathways due to reduced glycogen synthase and hexokinase activities, in the presence of an ongoing reduction of central obesity. We postulate that the insulin resistance is due to chronic rhGH-induced alterations in FFA metabolism, non-physiological levels of IGF-I and chronic basal hyperinsulinemia.
 ...
PMID:Insulin sensitivity in growth hormone (GH)-deficient adults and effect of GH replacement therapy. 1044 67

The direct correlation between glucose levels and cardiovascular disease in individuals with type 2 diabetes can now be applied to individuals that share an abnormal metabolic milieu similar to that found in central obesity, the metabolic syndrome, and type 2 diabetes. Premature macrovascular complications with a very high morbidity and mortality rate can be found in these nondiabetic populations. The typical phenotype has visceral or central obesity, excess of free fatty acids, insulin resistance, increased insulin secretion, and hypertension. A more complex metabolic-cardiovascular syndrome develops that includes dyslipidemia, abnormal production of cytokines, chronic inflammatory state, and abnormal coagulation. The interplay of all these cardiovascular risk factors is responsible for the accelerated atherosclerotic process. The different terminologies used for populations sharing this common ground for premature cardiovascular disease now generally accepted as the metabolic syndrome, are also discussed. Aggressive insulin treatment during acute illness in individuals with the abnormal metabolic milieu is beneficial. Insulin treatment is changing from using insulin as a hormone to treat only severe hyperglycemia, to a new paradigm using insulin in high doses as a drug. Aggressive insulin regimens should be used to treat only minimal elevations of blood glucose or to prevent hyperglycemia. The newly observed properties of insulin are reviewed which include suppression of inflammatory cytokines and adhesion molecules, improved hemostasis, and other cardiac beneficial effects. The concomitant administration of intravenous glucose and insulin permits the administration of higher insulin doses that can result in improved outcome due to its nonglycemic-related benefits. The use of aggressive insulin therapy requires both better and more cost-effective algorithms to successfully treat this high-risk population during acute illness.
 ...
PMID:Using insulin as a drug rather than as a replacement hormone during acute illness: a new paradigm. 1450 30

Patients with diabetes type 2 are not directly endangered by dysglycemia but they suffer vascular complications. The diabetic patient with existing cardiovascular disease has a particularly high risk for further cardiovascular complications and therefore requires specific attention. This is not only due to the hyperglycemia, but due to the coexistence of further cardiovascular risk factors, such as hypertension, dyslidemia, visceral fat accumulation, chronic inflammation and coagulopathy, also clinically described as the metabolic syndrome. These patients need an intense and multi-modal therapeutic approach, not only for improvement of glycemic control. Also other vascular risk factors should be handled aggressively, such as blood pressure, coagulopathy and dyslipidemia. Recent studies--as STENO 2--indicate that a multi-modal and aggressive approach in diabetic patients can markedly improve their prognosis. Therefore, the current practice of a glucocentric approach should be changed towards a more vascular approach.
 ...
PMID:[Pharmacotherapy of diabetes mellitus type 2. From the glucocentric tradition towards cardiovascular risk management]. 1652 15

Adhesion molecules play a significant role in leukocyte migration across the endothelium and are also involved in regulating immune system. It is shown that diabetic patients have an increase of soluble adhesion molecules (sICAM-1, sICAM-2, sVCAM-1, sE-selectin, sL-selectin, sP-selectin) considered an integral part of inflammatory state. This inflammation is responsible for the increased cardiovascular risk of these patients. There is a close link between hyperglycemia, oxidative stress, coagulopathy and inflammation and between these factors and the vascular damage. Various studies have showed the potential role of adhesion molecules in the pathogenesis of diabetic vasculopathy. They promote leukocyte recruitment, which is one of the initial steps in the genesis of atherosclerotic plaque. Adhesion molecules are also involved in the pathogenesis of diabetes mellitus type 1; sICAM-1 would have a particular immunomodulatory role in the process of destroying beta-cells and could be used as a subclinical marker of insulitis. Plasma levels of soluble adhesion molecules correlate with hyperglycemia, insulin resistance, dyslipidemia and obesity; they are associated with the development of nephropathy, retinopathy, myocardial infarction, stroke and obliterant peripheral arterial disease in diabetic type 1 and 2. Given the role of these molecules in endothelial dysfunction genesis and tissue damage associated with diabetes, they could constitute a therapeutic target for the prevention of genesis and progression of chronic complications of diabetic disease.
 ...
PMID:[Adhesion molecules and diabetes mellitus]. 2054 49

HIV infected patients are at increased risk for venous and arterial thromboembolic events. Multiple markers related to inflammation (IL-6, TNFrI, C-reative protein) and coagulation (tissue factor expression, FVIII, thrombin, fibrinogen and D-dimer levels) are increased in HIV infection, and several are predictive of thrombotic risk and mortality in HIV disease. The mechanisms behind the risk for abnormal coagulation in HIV infection have not been fully elucidated, but may be related to a chronic immune activation and inflammatory state in both untreated and treated HIV infection. The contribution of traditional risk factors, including smoking and dyslipidemia, overly represented in HIV infected patients, must also be considered when assessing thrombotic risk in this setting. Currently, several interventional studies are aimed at reducing inflammation and cardiovascular risk in HIV disease and may provide insights into the determinants of clotting events in HIV infected patients.
...
PMID:Coagulation and morbidity in treated HIV infection. 2475 34

Cushing's syndrome (CS), including visceral obesity, dyslipidemia, hypertension and diabetes among its many manifestations, is "a model" of metabolic syndrome. Glucocorticoid (GC) excess, through a combination of effects on liver, muscle, adipose tissue and pancreas, increases gluconeogenesis and impairs insulin sensitivity, leading to carbohydrate abnormalities. Dyslipidemia is a common finding in CS as a consequence of GC-related increased lipolysis, lipogenesis and adipogenesis. CS patients experience typical changes in body composition, with fat redistribution resulting in accumulation of visceral adipose tissue. Hypertension, myocardial and vascular abnormalities along with the metabolic changes and the characteristic coagulopathy increase cardiovascular morbidity and mortality. Metabolic syndrome features can persist long after normalisation of cortisol levels.
 ...
PMID:Metabolic Syndrome in Cushing's Syndrome Patients. 2989 89

The well-established relationship between diabetes and cardiovascular complications, combined with the rapidly increasing prevalence of diabetes, has created a pressing need for better understanding of the mechanisms of diabetic atherosclerosis. Multiple metabolic and diabetes-specific factors have been associated with accelerated atherosclerosis, including dyslipidemia, oxidative stress, inflammation, vascular cell dysfunction and coagulopathy. This discussion highlights selected studies in which researchers have employed mouse models of diabetic atherosclerosis in an attempt to examine these mechanisms and test potential therapeutic and preventative measures.
 ...
PMID:Macrovascular complications of diabetes in atherosclerosisprone mice. 3093 83


1 2 Next >>