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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The common clustering of glucose intolerance, insulin resistance, abdominal adiposity, elevated blood pressure, and low HDL cholesterol is referred to as metabolic syndrome. Individuals with this syndrome have an increased risk of developing cardiovascular disease (CVD). The World Health Organisation and the National Cholesterol Education Programme's Adult Treatment Panel III (NCEP-ATP III) have outlined specific diagnostic criteria for the diagnosis of the metabolic syndrome to help in the identification of this syndrome in clinical practice. While the WHO criteria were specifically developed for use in research, the NCEP criteria are useful in clinical diagnosis of the metabolic syndrome. The metabolic syndrome is amenable to lifestyle modifications such as increased physical activity, weight loss, and possibly intake of low-glycemic foods. Drug therapy may be used to treat individual components of the syndrome such as elevated blood pressure and dyslipidemia. To control elevated glucose levels (when there is failure of lifestyle modification), medications such as metformin, thiazolidinedione derivatives and alpha glucosidase inhibitors may be used.
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PMID:The metabolic syndrome: an emerging risk state for cardiovascular disease. 1523 Apr 89

The metabolic syndrome is a widespread clinical condition and an important cluster of atherothrombotic disease risk factors. The inclusion of this syndrome in the recently published Adult Treatment Panel III (ATP III) guidelines focused the attention of the physicians on this entity. Abdominal obesity, PPAR modulation, insulin resistance (with or without glucose intolerance), atherogenic dyslipidemia, elevated blood pressure, prothrombotic and proinflammatory states are the principal factors of this multifaceted syndrome. There are two major pathways of metabolic syndrome progress: (1) With preserved pancreatic beta cells function and insulin hypersecretion, which can recompense for insulin resistance. This pathway leads mostly to the macrovascular complications of metabolic syndrome. (2) With substantial injure of pancreatic beta cells leading to gradually reduced insulin secretion and to hyperglycemia (e.g. overt type 2 diabetes). This pathway leads to both microvascular and macrovascular complications. Because macrovascular complications of insulin resistance state precede the onset of hyperglycemia, early intervention in patients with metabolic syndrome is particularly important. Since central obesity (accompanied by insulin resistance even in the absence of hyperglycemia) is the key factor leading to development of metabolic syndrome and its future macrovascular complications, we assume that next logical step is the recognition of central obesity itself as a major risk factor for cardiovascular diseases.
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PMID:Macrovascular complications of metabolic syndrome: an early intervention is imperative. 1545 79

The diagnosis of metabolic syndrome is based on identification of the following parameters: abdominal obesity, triglycerides, HDL-cholesterol, blood pressure, fasting glycemia, as recommended by ATP III. In order to simplify the clinical practice, at least two parameters should be screened for. The most frequent couple, easy to be determined in practice, is hypertensive waist, followed by hypertriglyceridemic waist, hypertensive dyslipidemia, dysglycemic dyslipidemia and hypertensive dysglycemia. Based on these couples the next step would be to identify the triads that diagnose the metabolic syndrome. A global assessment of cardiovascular risk should be made. Suggested method is to apply the Framingham Score. Therapeutic intervention is structured according to levels of cardiovascular risk. Clinical management is structured on THEME Programs (therapy, education, monitoring, evaluation), applied to all risk factors.
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PMID:Metabolic syndrome--practical approach. 1552 14

The metabolic syndrome is diagnosed according to criteria set by either WHO (obesity, high blood pressure, dyslipidemia, insulin resistance) or more recently by ATP III (National Cholesterol Education Program's Adult Treatment Panel III report). The latter emphasizes abdominal obesity, atherogenic dyslipidemia, high blood pressure and increased fasting glucose. Without presuming a nosologic entity, the metabolic syndrome is emerging as by far the most important precursor of an epidemic of cardiovascular disease, not only in Western countries. This epidemic calls for action at a time when our understanding of dietary intervention for maintaining weight loss remains primitive and cannot withstand critical scrutiny (because of a lack of long term randomised, prospective studies). Dietary therapy in metabolic syndrome therefore has to be aimed where success is most likely, i.e. at a reduction in energy intake and increase in output by physical activity, a prudent balance of carbohydrates, proteins and fats, taking into account secondary changes in lipid profiles and the glycemic load of nutrients. All nutritional advice must be incorporated in long term programs with continuous guidance, preferably in group therapy targeting all individual risk factors.
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PMID:[Metabolic syndrome: diagnosis and dietary intervention]. 1733 58

The aim of this editorial was to discuss evidence indicating a role for low-grade inflammation as a pathogenetic event of the metabolic syndrome. The metabolic syndrome has emerged as an important cluster of risk factors for atherosclerotic disease. Common features are central (abdominal) obesity, insulin resistance, hypertension, and dyslipidemia, namely high triglycerides and low high-density lipoprotein cholesterol. According to the clinical criteria developed by ATP III, it has been estimated that 1 out of 4 adults living in the United States merits the diagnosis. The presence of the metabolic syndrome is highly prognostic of future cardiovascular events. Chronic inflammation may represent a triggering factor in the origin of the metabolic syndrome: stimuli such as overnutrition, physical inactivity, and ageing would result in cytokine hypersecretion and eventually lead to insulin resistance and diabetes in genetically or metabolically predisposed individuals. Alternatively, resistance to the anti-inflammatory actions of insulin would result in enhanced circulating levels of proinflammatory cytokines resulting in persistent low-grade inflammation. A generally enhanced adipose tissue derived cytokine expression may be another plausible mechanism for the inflammation/metabolic syndrome relationship. The role of adipose tissue as an endocrine organ capable of secreting a number of adipose tissue-specific or enriched hormones, known as adipokines, is gaining appreciation. Although the precise role of adipokines in the metabolic syndrome is still debated, an imbalance between increased inflammatory stimuli and decreased anti-inflammatory mechanisms may be an intriguing working hypothesis. The proinflammatory state that accompanies the metabolic syndrome associates with both insulin resistance and endothelial dysfunction, providing a connection between inflammation and metabolic processes which is highly deleterious for vascular functions.
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PMID:The metabolic syndrome and inflammation: association or causation? 1567 55

For examining whether dissipating excess energy in the liver is a possible therapeutic approach to high-fat diet-induced metabolic disorders, uncoupling protein-1 (UCP1) was expressed in murine liver using adenoviral vectors in mice with high-fat diet-induced diabetes and obesity, and in standard diet-fed lean mice. Once diabetes with obesity developed, hepatic UCP1 expression increased energy expenditure, decreased body weight, and reduced fat in the liver and adipose tissues, resulting in markedly improved insulin resistance and, thus, diabetes and dyslipidemia. Decreased expressions of enzymes for lipid synthesis and glucose production and activation of AMP-activated kinase in the liver seem to contribute to these improvements. Hepatic UCP1 expression also reversed high-fat diet-induced hyperphagia and hypothalamic leptin resistance, as well as insulin resistance in muscle. In contrast, intriguingly, in standard diet-fed lean mice, hepatic UCP1 expression did not significantly affect energy expenditure or hepatic ATP contents. Furthermore, no alterations in blood glucose levels, body weight, or adiposity were observed. These findings suggest that ectopic UCP1 in the liver dissipates surplus energy without affecting required energy and exerts minimal metabolic effects in lean mice. Thus, enhanced UCP expression in the liver is a new potential therapeutic target for the metabolic syndrome.
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PMID:Dissipating excess energy stored in the liver is a potential treatment strategy for diabetes associated with obesity. 1567 88

Lipoprotein abnormalities are present in a high proportion of renal transplant patients. It is accepted that dyslipidemia is associated with atherosclerosis and in the progression of renal disease. Lipid abnormalities may also play a significant role in the development of chronic allograft nephropathy. Sirolimus was found to have an antiatherosclerotic effect in the apolipoprotein E-knockout mice model of hyperlipidemia through its antiproliferative effects. As lipid-mediated renal injury is important in the pathogenesis of glomerulosclerosis which shares common pathogenic mechanisms with atherosclerosis, in this study we have tested the hypothesis that sirolimus prevents lipid-mediated renal injury through the modulation of cholesterol homeostasis of mesangial cells and its anti-inflammatory effects on macrophages. We demonstrated that sirolimus reduced lipid accumulation, as measured by oil red O staining in human mesangial cells (HMCs). Using real-time PCR, we screened the mRNA expression of lipoprotein receptors. Sirolimus significantly suppressed LDL and VLDL receptors and CD36 gene expression. It also increased cholesterol efflux from HMCs by increasing peroxisome proliferator-activated receptor-alpha (PPARalpha), PPARgamma, liver X receptor-alpha, and ATP binding cassette A1 (ABCA1) gene expression. Sirolimus overrode the suppression of cholesterol efflux and ABCA1 gene expression induced by the inflammatory cytokine IL-1beta. Furthermore, sirolimus significantly inhibited inflammatory cytokines IL-6 and TNF-alpha production in macrophages. These data suggest that sirolimus may prevent cellular cholesterol accumulation even in the presence of hyperlipidemia and inflammation, by regulating both cholesterol homeostasis and inflammatory responses.
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PMID:Effects of sirolimus on mesangial cell cholesterol homeostasis: a novel mechanism for its action against lipid-mediated injury in renal allografts. 1576 38

A clustering of insulin resistance, hypertension and dyslipidemia has been labeled as the metabolic syndrome. Asians have a lower frequency of obesity than do Caucasians, but have an increasing tendency toward metabolic syndrome. Most data on metabolic syndrome are based on studies from Western countries with only limited information derived from Asian populations. We conducted a cross-sectional study of individuals aged 30-60 yr in workplace settings. We examined and analyzed the health data of 1,384 Japanese, Koreans and Mongolians for metabolic syndrome based on the modified definitions of the working definition proposed by the Third Report of the National Cholesterol Educational Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (ATP III definition). The prevalence of metabolic syndrome using the ATP III-BMI30 and ATP III-BMI25 definitions was 7% and 12% for Japanese, 7% and 13% for Koreans, and 12% and 16% for Mongolians, respectively. With the exception of obesity, the prevalences of individual metabolic abnormalities within each of the three Asian groups were similar to each other and to reported rates of prevalence in the U.S.A. Nevertheless, the values of sensitivity and specificity by the metabolic syndrome definitions are remarkably different relative to ethnicity. A universal metabolic syndrome definition is inappropriate for comparisons of metabolic syndrome among Asian ethnic groups. We believe that the ATP III-BMI25 definition is suitable for the determination of metabolic syndrome among Japanese and Koreans, and that the ATP III-BMI30 is more appropriate for Mongolians.
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PMID:Prevalence of the metabolic syndrome using the modified ATP III definitions for workers in Japan, Korea and Mongolia. 1582 77

Lipid abnormalities play an important part in raising the cardiovascular risk in diabetic subjects. The main components of diabetic dyslipidemia are increased plasma triglycerides, low concentration of high-density lipoprotein cholesterol, preponderance of small, dense low-density lipoprotein, and excessive postprandial lipemia. Small, dense low-density lipoprotein, the elevation in remnant triglyceride-rich lipoprotein particles, and the low high-density lipoprotein are the most powerful atherogenic components. The coexistence of these three factors strongly aggravates the lipid accumulation in the arterial wall and the formation of atherosclerotic plaques. The position of diabetes in cardiovascular risk assessment has been recently reviewed in the Harmonized Clinical Guidelines on Prevention of Atherosclerotic Vascular Disease. In general, patients with diabetes carry a high risk for cardiovascular disease, but the absolute risk varies depending on the type of diabetes, age, and population baseline risk. The Adult Treatment Program III (ATP III) and the American Heart Association have designated diabetes as a high-risk condition and recommended intensive risk-factor management. Concerning therapeutic targets, both ATP III and the American Diabetes Association (ADA) guidelines have identified low-density lipoprotein cholesterol as the first priority of lipid lowering, and the optimal level was set at less than 2.6 mmol/L (100 mg/dL). There is strong evidence, coming from landmark secondary prevention studies, that LDL lowering in people with diabetes is associated with significant clinical benefits. The benefits of statin therapy in type 2 diabetics can no longer be questioned. Ongoing clinical trials will help clarify the question of whether increasing high-density lipoprotein cholesterol with fibrates in the presence of low low-density lipoprotein levels (lower than 3.4 mmol/L, or 130 mg/dL) will be more beneficial than statin therapy alone. The new paradigms in risk-reduction therapies for type 2 diabetic subjects are focused on cardiovascular disease prevention, rather than only on glucose or lipid control. Therapeutic lifestyle changes are considered primary therapies for hyperglycemia and coexisting metabolic syndrome, which can be diagnosed in more than half of type 2 diabetes subjects. New perspectives of lipid management in type 2 diabetes should take into account that insulin resistance, increased lipolysis, and overproduction of large, buoyant, very low density lipoprotein particles are at the base of diabetic dyslipidemia. Accordingly, drugs acting in the regulatory steps of very low density lipoprotein assembly should be developed. Activation of peroxisome proliferator activated receptor alpha (PPARalpha), as occurs with fibrates, lowers free fatty acids (FFAs) and triglyceride levels. PPARgamma agonism, as demonstrated by the thiazolidinediones, increases triglyceride lipolysis, FFA transport, and conversion of FFAs to triglycerides. As separate activation of PPARalpha and PPARgamma improves lipid metabolism, the development of new drugs integrating PPARalpha and PPARgamma activity (PPAR-alpha/gamma agonists) is a promising line that may further improve insulin resistance, FFA metabolism, and consequently, atherogenic diabetic dyslipidemia.
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PMID:Statins and diabetes. 1586 14

Studies have highlighted the association between insulin resistance (IR) and several cardiovascular (CV) risk factors, including hypertension (HTN), obesity, dyslipidemia (i.e. high triglyceride and low HDL-cholesterol) and glucose intolerance, in a cluster known as the metabolic syndrome (MS). There are few data on the frequency of the MS and dyslipidemia in developing countries, and none in South America. To estimate the prevalence of the MS and its components in Zulia State, Venezuela, and to establish associated demographic and clinical factors, we evaluated 3108 Hispanic men and women aged 20 years or older from a cross-sectional survey of a random representative sample from each health district in Zulia State, Venezuela (1999-2001). Prevalence of the MS and dyslipidemia was defined according to the National Cholesterol Education Program (NCEP)/Adult Treatment Panel III (ATP III) criteria. The age-adjusted prevalence of MS and dyslipidemia was 31.2% and 24.1%, respectively, with higher rates in men than in women. Prevalence rates increased with age and with the degree of obesity. MS prevalence was lower in Amerindian (17.%) compared to Black (27.2%), White (33.3%) and Mixed (37.4%) men, but no differences were found among women. Overall, low HDL-cholesterol (65.3%), abdominal obesity (42.9%) and HTN (38.1%) were the most frequent MS components. After adjusting for age, sex and race groups, family history of diabetes, obesity and HTN were associated with the MS. Sedentary lifestyle also increased the risk of MS, event after adjusting for the same covariates, obesity and the degree of IR. These results suggest that MS is found in approximately one-third of the Venezuelan adult population in Zulia State, with higher prevalence in men related to the presence of dyslipidemia. Lifestyle interventions in MS subjects are needed in Venezuela to halt the burden of CV disease and diabetes.
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PMID:Prevalence and risk factors associated with the metabolic syndrome and dyslipidemia in White, Black, Amerindian and Mixed Hispanics in Zulia State, Venezuela. 1595 88


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