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

The roles of polymorphisms of the sitosterolemia genes ABCG5 and ABCG8 in the regulation of cholesterol metabolism and insulin sensitivity were studied in mildly hypercholesterolemic noncoronary subjects (n = 263, 144 men and 119 women) divided into tertiles by baseline serum cholestanol-to-cholesterol ratio (< or = 118.3 and > or = 147.7 10(2) x mmol/mol cholesterol), a surrogate marker of cholesterol absorption efficiency. The lowest cholestanol tertile was associated with high body mass index (BMI), plasma glucose, serum insulin and triglycerides, and cholesterol synthesis markers (cholestenol, desmosterol, lathosterol) and low HDL cholesterol and cholesterol absorption markers (campesterol, sitosterol) (P < 0.01 for all). The 19H allele of the ABCG8 gene accumulated in the lowest cholestanol tertile (P < 0.001) and was associated with low total and LDL cholesterol and absorption markers and with high synthesis markers (P < 0.05 for all). The 604E allele of the ABCG5 gene in men was associated with high BMI, plasma insulin, low serum sitosterol, and high serum cholestenol levels (P < 0.05 for all). In a subgroup of 71 men, the 604E allele was associated with insulin resistance measured with the hyperinsulinemic euglycemic clamp. In conclusion, low cholesterol absorption efficiency was associated with characteristics of the metabolic syndrome. Low serum cholesterol and cholesterol absorption were linked to the D19H polymorphism of the ABCG8 gene, and characteristics of the insulin resistance syndrome in men were linked with the Q604E polymorphism of the ABCG5 gene.
J Lipid Res 2004 Sep
PMID:Polymorphisms in the ABCG5 and ABCG8 genes associate with cholesterol absorption and insulin sensitivity. 1517 52

The metabolic syndrome encapsulates visceral obesity, insulin resistance, diabetes, hypertension and dyslipidaemia. Dyslipidaemia is a cardinal feature of the metabolic syndrome that accelerates the risk of cardiovascular disease. It is usually characterized by high plasma concentrations of triacylglycerol (triglyceride)-rich and apoB (apolipoprotein B)-containing lipoproteins, with depressed concentrations of HDL (high-density lipoprotein). However, lipoprotein metabolism is complex and abnormal plasma concentrations can result from alterations in the rates of production and/or catabolism of these lipoprotein particles. Our in vivo understanding of kinetic defects in lipoprotein metabolism in the metabolic syndrome has been achieved chiefly by ongoing developments in the use of stable isotope tracers and mathematical modelling. This review deals with the methodological aspects of stable isotope kinetic studies. The design of in vivo turnover studies requires considerations related to stable isotope tracer administration, duration of sampling protocol and interpretation of tracer data, all of which are critically dependent on the kinetic properties of the lipoproteins under investigation. Such models provide novel insight that further understanding of metabolic disorders and effects of treatments. Future investigations of the pathophysiology and therapy of the dyslipoproteinaemia of the metabolic syndrome will require the development of novel kinetic methodologies. Specifically, new stable isotope techniques are required for investigating in vivo the turnover of the HDL subpopulation of particles, as well as the cellular efflux of cholesterol into the extracellular space and its subsequent transport in plasma and metabolic fate in the liver.
Clin Sci (Lond) 2004 Sep
PMID:Lipoprotein transport in the metabolic syndrome: methodological aspects of stable isotope kinetic studies. 1522 43

The accompanying review in this issue of Clinical Science [Chan, Barrett and Watts (2004) Clin. Sci. 107, 221-232] presented an overview of lipoprotein physiology and the methodologies for stable isotope kinetic studies. The present review focuses on our understanding of the dysregulation and therapeutic regulation of lipoprotein transport in the metabolic syndrome based on the application of stable isotope and modelling methods. Dysregulation of lipoprotein metabolism in metabolic syndrome may be due to a combination of overproduction of VLDL [very-LDL (low-density lipoprotein)]-apo (apolipoprotein) B-100, decreased catabolism of apoB-containing particles and increased catabolism of HDL (high-density lipoprotein)-apoA-I particles. These abnormalities may be consequent on a global metabolic effect of insulin resistance, partly mediated by depressed plasma adiponectin levels, that collectively increases the flux of fatty acids from adipose tissue to the liver, the accumulation of fat in the liver and skeletal muscle, the hepatic secretion of VLDL-triacylglycerols and the remodelling of both LDL (low-density lipoprotein) and HDL particles in the circulation. These lipoprotein defects are also related to perturbations in both lipolytic enzymes and lipid transfer proteins. Our knowledge of the pathophysiology of lipoprotein metabolism in the metabolic syndrome is well complemented by extensive cell biological data. Nutritional modifications may favourably alter lipoprotein transport in the metabolic syndrome by collectively decreasing the hepatic secretion of VLDL-apoB and the catabolism of HDL-apoA-I, as well as by potentially increasing the clearance of LDL-apoB. Several pharmacological treatments, such as statins, fibrates or fish oils, can also correct the dyslipidaemia by diverse kinetic mechanisms of action, including decreased secretion and increased catabolism of apoB, as well as increased secretion and decreased catabolism of apoA-I. The complementary mechanisms of action of lifestyle and drug therapies support the use of combination regimens in treating dyslipoproteinaemia in subjects with the metabolic syndrome.
Clin Sci (Lond) 2004 Sep
PMID:Lipoprotein transport in the metabolic syndrome: pathophysiological and interventional studies employing stable isotopy and modelling methods. 1522 21

Protein tyrosine phosphatase 1beta (PTP-1beta) is involved in the regulation of several important physiological pathways. It regulates both insulin and leptin signaling, and interacts with the epidermal- and platelet-derived growth factor receptors. The gene is located on human chromosome 20q13, and several rare single nucleotide polymorphisms (SNPs) have been shown to be associated with insulin resistance and diabetes in different populations. As part of our ongoing investigations into the genetic basis of hypertension, we examined common sequence variants in the gene for association with hypertension, obesity and altered lipid profile in two populations of Japanese and Chinese descent. We re-sequenced all exons, selected intronic sequences and the promoter region in 24 individuals from our cohort. Fourteen SNPs were discovered, and six of these spanning 78 kb were genotyped in 1553 individuals from 672 families. All six SNPs were in linkage disequilibrium, and we found strong association of common risk haplotypes with hypertension in Chinese and Japanese (P<0.0001). In addition, individual SNPs showed association to total plasma cholesterol, LDL-cholesterol and VLDL-cholesterol levels, as well as obesity measures (body mass index). This analysis supports that PTP-1beta affects plasma lipid levels, and may lead to obesity and hypertension in Japanese and Chinese. Given similar associations found in other populations to insulin resistance and diabetes, this gene may play a crucial role in the development of the characteristic metabolic changes seen in patients with the metabolic syndrome.
Hum Mol Genet 2004 Sep 01
PMID:Single nucleotide polymorphisms in protein tyrosine phosphatase 1beta (PTPN1) are associated with essential hypertension and obesity. 1522 88

The metabolic syndrome as currently defined by the Adult Treatment Panel III includes multiple components. This article describes the background for these components' inclusion in the syndrome,measurement of these factors, and the appropriate interventions. The factors are highly interrelated and the true utility of this diagnostic entity is under critical evaluation as new and existing data are evaluated concerning the role of the syndrome in the development of vascular disease and other clinical outcomes.
Endocrinol Metab Clin North Am 2004 Sep
PMID:Estimating cardiovascular disease risk and the metabolic syndrome: a Framingham view. 1526 91

This article emphasizes the importance of weight reduction in obese individuals as the main nutritional focus relevant to the metabolic syndrome. Although other nutrients influence insulin sensitivity, these effects are modest in comparison with the benefit achievable with weight reduction. This article therefore initially discusses the dramatic rise in the prevalence of the metabolic syndrome,especially in the Asian-Pacific region where insulin resistance and the high conversion rate to type 2 diabetes are almost certainly related to weight gain.
Endocrinol Metab Clin North Am 2004 Sep
PMID:Nutritional aspects in the causation and management of the metabolic syndrome. 1526 92

The National Cholesterol Education Program's Adult Treatment Panel III identifies persons with multiple metabolic risk factors or "metabolic syndrome" as candidates for intensified therapeutic lifestyle changes. This article reviews the important role of weight reduction,diet, and exercise in improving the metabolic syndrome and its risk factors of abdominal obesity, impaired fasting glucose,dyslipidemia, and coagulation/inflammatory factors. The article also provides practical strategies.
Endocrinol Metab Clin North Am 2004 Sep
PMID:Focus on lifestyle change and the metabolic syndrome. 1526 93

Individuals who have the metabolic syndrome are at increased risk for cardiovascular disease. Combined dyslipidemia is an important component of metabolic syndrome, contributing to excess cardiovascular risk. Lifestyle and pharmacologic interventions are warranted for effective management of this syndrome. This article discusses the current evidence supporting the use of statins and their beneficial impact on lipid and nonlipid aspects of metabolic syndrome-related pathology.
Endocrinol Metab Clin North Am 2004 Sep
PMID:Management of metabolic syndrome: statins. 1526 94

Atherogenic dyslipidemia is prevalent in various conditions associated with central obesity, hypertension, hyperurecemia, and impaired beta-cell function (ie, the metabolic syndrome). Because of clinical trial evidence, most high-risk patients with atherogenic dyslipidemia require statin therapy. Coadministration of drugs targeted to reduction of low-density lipoprotein precursors, however,is likely to improve the metabolic profile of all non-high-density lipoproteins and produce a significant rise in high-density lipoprotein cholesterol. Large-scale clinical trials with combined drug therapy that show coronary heart disease (CHD) risk reduction or improvement in CHD are needed. It is also possible that new drugs are needed to target fatty acid metabolism and inflammation. As understanding of the metabolic origins of atherogenic dyslipidemia increases, it is possible that new targets of therapy will be identified and that new drug combinations will prove to be even more efficacious than those currently available for treatment of this condition.
Endocrinol Metab Clin North Am 2004 Sep
PMID:Management of atherogenic dyslipidemia of the metabolic syndrome: evolving rationale for combined drug therapy. 1526 95

There is increasing evidence that fibrates can reduce coronary artery disease. This finding seems to be particularly the case inpatients with the metabolic syndrome or with diabetes. Their beneficial effects can be explained partly by their effects on lipoproteins,but these effects may also result from some of their nonlipid pleotropic effects. Clinical trials are still needed to determine the potential role played by such pleotropic actions.
Endocrinol Metab Clin North Am 2004 Sep
PMID:Fibrates in the metabolic syndrome and in diabetes. 1526 96


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