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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A successful dietary strategy should reduce coronary heart disease (CHD) endpoints, improve correctable risk factors for CHD, and provide for an overall healthful lifestyle. The therapeutic diet achieves a lowering of low-density lipoprotein cholesterol by limiting saturated fat and dietary cholesterol, avoiding an increase in trans fatty acids, and incorporates the use of dietary adjuncts such as an increase in dietary viscous fiber and dietary plant stanol/sterol esters. For those with elevated triglycerides and low high-density lipoprotein cholesterol, impaired fasting glucose, increased waist circumference and other stigmata of the metabolic syndrome, individualized and supervised weight loss, and regular physical activity is strongly recommended.
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PMID:The optimal dietary strategy to manage risk associated with various dyslipidemias. 1150 76

Prevalence of coronary heart disease (CHD), of type 2 diabetes (T2DM) and of the metabolic syndrome are in Mauritius amongst the highest in the world. As T2DM and CHD are closely associated and have both a polygenic basis, we conducted a 10 cM genome scan with 403 microsatellite markers in 99 independent families of North-Eastern Indian origin including 535 individuals. Families were ascertained through a proband with CHD before 52 years of age and additional sibs with myocardial infarction (MI) or T2DM. Model-free two-point and multipoint linkage analysis were performed using the Mapmarker-Sibs (MLS) and maximum-likelihood-binomial (MLB) programs for autosomal markers and the Aspex program for chromosome X markers. In a second step, additional markers were studied to increase the genetic map density in three regions on chromosomes 3, 8 and 16 where initial indication for linkage was found. Our data show suggestive linkage with CHD on chromosome 16p13-pter with the MLS statistics at 8.69 cM (LOD = 3.06, P = 0.00017) which partially overlaps with a high pressure (HBP) peak. At the same locus, a nominal indication for linkage with T2DM was found in 35 large T2DM Pondicherian families also having Indian origin. With respect to region 8q23, we found suggestive linkage with T2DM (LOD = 2.55, P = 0.00058) as well as with HBP. On 3q27, we replicated previous indication for linkage found in Caucasians (for the metabolic syndrome and for diabetes) according to the categorized trait for CHD and MI with the MLB statistics (LOD = 2.13, P = 0.0009). The genome scan also revealed nominal evidence of linkage with CHD on 10q23 (LOD = 2.06, P = 0.00188). Interestingly, we detected in the same region overlapping linkages with three QTLs: age of onset of CHD (LOD = 2.03), HDL cholesterol (LOD = 1.48) and LDL/HDL ratio (LOD = 1.34). Ordered-subset analysis based on family body mass index ranking replicated finding on 2q37 for T2DM (at Calpain 10 locus). These results show the first evidence for susceptibility loci that predispose to CHD, T2DM and HBP in the context of the metabolic syndrome.
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PMID:A genome-wide scan for coronary heart disease suggests in Indo-Mauritians a susceptibility locus on chromosome 16p13 and replicates linkage with the metabolic syndrome on 3q27. 1173 40

Inflammation plays a key role in the physiopathology of atherosclerosis. C-reactive protein (CRP) has been found to predict cardiac events in healthy subjects and in patients with coronary heart disease. However, the relationship between CRP and subclinical atherosclerosis is not well established. We examined the potential relationship between CRP and common carotid artery intima-media thickness and carotid plaques in dyslipidemic subjects. Dyslipidemic patients (n=1051) were recruited for the study. All patients had a complete clinical examination and systematically underwent ultrasonographic evaluation of the extracranial carotid arteries on a duplex system. The serum concentration of CRP was measured by using a sensitive immunoradiometric assay. In a univariate model, a strong positive relationship was found between CRP and the severity of carotid stenosis (P<0.0001). In multivariate analysis, the association between CRP and the degree of carotid atherosclerosis remained significant for advanced plaques (P=0.0007) in male subjects only. Significant correlations were found between CRP and body mass index (P<0.0001) and between CRP and other markers associated with the metabolic syndrome. In this large dyslipidemic population, elevated CRP is an independent predictor of advanced carotid plaques in male subjects. Body mass index and other markers of the metabolic syndrome (HDL cholesterol, triglycerides, diabetes, and high blood pressure) are significant determinants of CRP levels in this population.
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PMID:Elevated C-reactive protein constitutes an independent predictor of advanced carotid plaques in dyslipidemic subjects. 1174 71

Nonalcoholic steatohepatitis (NASH) is a syndrome frequently associated with obesity, diabetes mellitus, and dyslipidemia. Increased fasting insulinemia and blood glucose levels may trigger a reduced catabolism of lipoproteins rich in triglycerides by lipoprotein lipase (LPL) and an increase in their fasting and postprandial levels. An association between postprandial lipemia and coronary heart disease has been observed, and many studies now support this concept. The most important result of our study is the increase in triglyceride-rich lipoproteins response after a fat load in NASH patients, the increase of incremental area under the postprandial curve, and the duration of the hypertriglyceridemic peaks. The persisting postprandial plasma triglyceride elevation in NASH patients was mostly due to the elevated plasma level of large triglyceride-rich particles. These data are coupled with lower plasma HDL2-cholesterol levels. As for lipoprotein analyses, the number of apolipoprotein B100 (ApoB100) particles is not significantly different between the two groups, and the higher content of triglycerides in NASH very low density lipoproteins (VLDL) increases the triglyceride-to-ApoB ratio and the particle size. A decreased enzymatic activity of LPL or a defective assembly and secretion of VLDL from hepatocytes due to a moderate reduction in microsomal triglyceride transfer protein could be involved in the overloading of VLDL. Moreover, the undetectable levels of ApoB48 in triglyceride-rich lipoproteins fraction A could be related to the synthesis of smaller and denser chylomicrons. NASH patients not only are insulin resistant but also tend to present alterations in fatty meal delivery, suggesting that an increase in fasting plasma insulin and glucose, with insulin resistance, joins with depressed metabolism of triglyceride-rich lipoproteins. An increase in postprandial triglyceride levels with production of large VLDL suggests an atherogenic behavior of lipid metabolism, in accordance with the high prevalence of the metabolic syndrome in NASH patients. This paper suggests that a fat load may be useful in early detection of atherogenic risk in the presence of otherwise normal fasting plasma lipids.
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PMID:Postprandial triglyceride-rich lipoprotein metabolism and insulin sensitivity in nonalcoholic steatohepatitis patients. 1176 56

Compelling evidence from meta-analysis of a number of clinical studies on a large aggregate of patients has established an increased level of triglycerides as an independent risk factor for atherosclerotic heart disease. The finding of triglyceride-rich lipoproteins in human atheromata has provided substantial pathophysiologic evidence for a direct role in atherogenesis. Hypertriglyceridemia is commonly embedded in the context of a metabolic syndrome that includes central obesity, insulin resistance, low levels of HDL cholesterol, and often hypertension. Hypertriglyceridemia also appears to underlie the phenomenon of small dense LDL in most instances. Therapeutic interventions must be directed at underlying obesity, insulin resistance, and diabetes when present, as well as addressing metabolic determinants of dyslipidemia per se. Diet, exercise, weight loss, and avoidance of alcohol are the cornerstones of treatment. The choice of medication should be based on the lipoprotein phenotype. Niacin, fibric acid derivatives, and omega-3 fatty acids are most useful in treating severe hypertriglyceridemia. HMG-CoA reductase inhibitors are useful in some phenotypes with moderately increased triglyceride levels. Evidence from a number of clinical trials indicates that mitigation of risk of coronary heart disease, and possibly stroke, can be effected by reducing levels of plasma triglycerides.
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PMID:A risk factor for atherosclerosis: triglyceride-rich lipoproteins. 1179 72

Type 2 diabetes is increasingly recognized as a major risk factor for coronary heart disease (CHD). The recent Adult Treatment Panel III of the National Cholesterol Education Program makes special mention of diabetes and the metabolic syndrome and proposes a secondary goal of therapy following achievement of the LDL goal, namely non-HDL cholesterol (the sum of VLDL and LDL cholesterol, i.e. total cholesterol-HDL cholesterol). In addition diabetes is recognized as a CHD risk equivalent. Much information is available from subgroup analysis of the major CHD secondary prevention trials of lipid-lowering with regard to the benefits for diabetic patients. However little information is available from clinical trials in primary prevention. Ongoing trials will help fill this gap. Recently the first report of a large lipid-lowering trial addressing coronary atherosclerosis in a specific diabetic population has been published-the Diabetes Atherosclerosis Intervention Study (DAIS). In this study fenofibrate therapy was associated with reduced progression of coronary atherosclerosis assessed by quantitative coronary angiography.
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PMID:Lipid-lowering trials in diabetes. 1180 61

The importance of the obesity-lipid connection has suffered from the traditional reductionism view of science. Excess body weight has rarely been deemed an independent risk factor for coronary heart disease, directing physicians to target therapies towards the risk factors that excess body weight modifies (e.g. raising HDL, lowering blood pressure) instead of targeting the cause. The efforts of Adult Treatment Panel III to define and identify the metabolic syndrome as a secondary target may spur practitioners to revisit the need for weight management in patients with lipid disorders.
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PMID:Connections between obesity and dyslipidaemia. 1180 62

The purpose of this review is to consider how current animal models of fetal programming contribute to knowledge of the metabolic syndrome in adult humans. Low birth weight infants have an increased risk of developing cardiovascular and coronary heart disease, hypertension, diabetes and stroke in adulthood. A number of animal studies confirm the association between events during fetal life and subsequent adult disease. This review considers how these have contributed to our understanding of this relationship, and how they may help to uncover the underlying mechanisms. The importance of dietary, pharmacological, genetic and surgical models is assessed, and their usefulness in the prevention of human disease evaluated. Although progress has been made, further investigations using animals are needed to clarify the mechanisms involved in the programming of adult disease. Once these processes are understood, it may be possible to identify and protect at-risk individuals.
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PMID:Animal models and programming of the metabolic syndrome. 1180 21

Epidemiologic studies have consistently implicated low plasma high-density lipoprotein cholesterol as an important, independent risk factor for the development of coronary heart disease. However, clinical trials specifically designed to evaluate the role of lipid therapy in patients with low high-density lipoprotein cholesterol have only been recently reported. They include two trials with angiographic end points, the Lopid Coronary Angiography Trial and the Bezafibrate Coronary Atherosclerosis Intervention Trial, and three clinical end points trials, the Air Force/Texas Coronary Atherosclerosis Prevention study, the Department of Veterans Affairs High-Density Lipoprotein Intervention Trial, and the Bezafibrate Infarction Prevention study. These and other trials clearly indicate that persons with coronary heart disease and high low-density lipoprotein cholesterol (>130 mg/dL [3.36 mmol/L]), with or without low high-density lipoprotein cholesterol, benefit from statin therapy. The Air Force/Texas Coronary Atherosclerosis Prevention study showed that persons at high risk of coronary heart disease but without known disease, who have moderate levels of low-density lipoprotein cholesterol as well as low levels of high-density lipoprotein cholesterol, also appear to benefit from statin therapy although the cost effectiveness of this approach is unclear. The results from the Department of Veterans Affairs High Density Lipoprotein Intervention Trial provide convincing evidence that patients without high low-density lipoprotein cholesterol and with established coronary heart disease and low high-density lipoprotein cholesterol benefit from gemfibrozil. This drug may be particularly beneficial for patients who, in addition to low high-density lipoprotein cholesterol, present with other features of the metabolic syndrome, such as obesity, glucose intolerance, and high triglycerides. Whether other fibrates, niacin, or statins lower coronary heart disease risk in persons with low high-density lipoprotein cholesterol in the absence of high or moderately high low-density lipoprotein cholesterol is unknown. (c)2000 by CHF, Inc.
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PMID:High-density lipoprotein and coronary heart disease: lessons from recent intervention trials. 1183 14

The third set of guidelines recently issued by the National Cholesterol Education Program (NCEP) differs from the second set issued in 1993 in several ways. The third set introduced a quantitative risk scoring system and identified and/or reclassified certain groups of patients at high or moderate risk for a coronary event. Among these groups are patients with type 2 diabetes, and patients with multiple risk factors other than coronary heart disease or diabetes that cumulatively confer high risk for a coronary event. However, the new guidelines also present physicians with the major challenges of identifying these patients, determining their true risk, and implementing the recommended approaches to treatment in clinical practice settings. Although reducing elevated levels of low-density lipoprotein (LDL) cholesterol remains the primary focus of therapy, the new NCEP guidelines also include strategies to identify and treat patients with low levels of high-density lipoprotein (HDL) cholesterol and/or elevated triglyceride levels. Just as there is "good" cholesterol (HDL) and "bad" cholesterol (LDL), there are also "good" triglycerides, which contain high concentrations of triglyceride remnants and are associated with low risk, and "bad" triglycerides, which contain high concentrations of cholesterol remnants and are associated with increased risk. The mechanisms by which "bad" triglycerides develop explain why elevated triglycerides and low HDL--and patients with the metabolic syndrome--warrant special attention. These mechanisms and others also suggest new targets for therapeutic intervention and the development of new drugs that will correct lipid and lipoprotein abnormalities through a number of different metabolic pathways.
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PMID:Rising to the challenge of the new NCEP ATP III guidelines: exceeding current therapeutic limitations. 1185 98


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