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

There are now five placebo-controlled trials of EPA in the treatment in schizophrenia, and four of these have given positive or partly positive findings. A cross-national ecological analysis of international variations in outcome of schizophrenia in relation to national dietary practices, showed that high consumption of sugar and of saturated fat is associated with a worse long-term outcome of schizophrenia. It is known that a high sugar, high fat diet leads to reduced brain expression of brain-derived neurotrophic factor (BDNF) which is responsible for maintaining the outgrowth of dendrites. Low brain BDNF levels also lead to insulin resistance which occurs in schizophrenia and is associated with diseases of the metabolic syndrome. It appears that the same dietary factors which are associated with the metabolic syndrome, including high saturated fat, high glycaemic load, and low omega-3 PUFA, may also be detrimental to the symptoms of schizophrenia, possibly through a common mechanism involving BDNF.
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PMID:Nutrition and schizophrenia: beyond omega-3 fatty acids. 1504 Oct 37

Increase in triglyceride (TG) -rich lipoproteins is one of the symptoms clustered in metabolic syndrome and is associated with increased plasma free fatty acid level derived from central obesity and insulin resistance. Increase in triglyceride (TG) -rich lipoproteins is also related to several coronary risk factors such as remnant hyperlipidemia, decreased HDL-cholesterol, elevated small dense LDL, postprandial hyperlipidemia, and hypercoagulability. The first line of treatment for hypertriglyceridemia is the modification of individual life-style, among which, restriction of over-eating and practice of regular exercise are both essential. The consideration of dietary composition, not only the quantity but also the quality of nutrients, such as fat and carbohydrate, and behavior toward diet are also important to manage abnormal lipid profile. Statins, fibrates, nicotinic acid derivatives, and EPA are the drugs recommended for the treatment of dyslipidemias in metabolic syndrome.
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PMID:[Clinical significance of triglyceride-rich lipoproteins in metabolic syndrome]. 1759 89

The human metabolic syndrome and its frequent sequela, type 2 diabetes are epidemic around the world. Alpha-linolenic acid (ALA, 18:3 n-3), eicosapentaenoic acid (EPA, 20:5 n-3) and docosahexaenoic acid (DHA, 22:6 n-3) consumption ameliorates some of these epidemics' features thus leading one to question if consumption of EPA and DHA, and their metabolic precursor ALA reduce the conversion of metabolic syndrome to type 2 diabetes and reduce the major cause of death in the metabolic syndrome and type 2 diabetes-myocardial infarction. Contributing to myocardial infarction are metabolic syndrome's features of dyslipidemia (including elevated total cholesterol and LDL-c), oxidation, inflammation, hypertension, glucose intolerance, overweight and obesity. Inflammation, glucose and lipid levels are variously influenced by disturbances in various adipocytokines which are in turn positively impacted by n-3 polyunsaturated fatty acid consumption. Type 2 diabetes has all these features though elevated total cholesterol and LDL-c are rarer. It is concluded that EPA and DHA consumption significantly benefits metabolic syndrome and type 2 diabetes primarily in terms of dyslipidemia (particularly hypertriglyceridemia) and platelet aggregation with their impact on blood pressure, glucose control, inflammation and oxidation being less established. There is some evidence that EPA and/or DHA consumption, but no published evidence that ALA reduces conversion of metabolic syndrome to type 2 diabetes and reduces death rates due to metabolic syndrome and type 2 diabetes. ALA's only published significance appears to be platelet aggregation reduction in type 2 diabetes.
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PMID:The role of consumption of alpha-linolenic, eicosapentaenoic and docosahexaenoic acids in human metabolic syndrome and type 2 diabetes--a mini-review. 1789 98

Insulin Resistance along with endothelial dysfunction give rise to a constellation of syndromes designated as IRS/MBS metabolic syndrome. Endothelial dysfunction starts early in life much before the development of structural atherosclerosis. Recent insights into vascular biology enable us to understand the molecular mechanisms underlying endothelial dysfunction, and the scope and need for prevention of "pre-clinical" coronary atherosclerosis through lifestyle modification; diet, exercise and stress management. Diminished production of nitric oxide (NO) and/or increased inactivation of NO through oxidative stress (reactive oxygen species ROS and reactive nitrogen species (RNS) are the basis of endothelial dysfunction hence increasing the bioavailability of NO and decreasing its inactivation is the aim of prevention and reversal of endothelial dysfunction. Insulin regulates constitutive NOS gene expression in endothelial cells in vivo; vasodilation is an important component of Insulin-stimulated whole body glucose uptake. Successful strategies are: PPAR alpha and gamma agonists which increase NO production in endothelium; anti-oxidants such as vit. E and C; supplementation with L-arginine, tetrahydrobiopterin-BH4 or sepiapterin (precursor of BH4), SOD mimetic tempol, statins which apart from lowering cholesterol improve NO production, selective beta1 adrenoreceptor antagonists such as nebivolol; suppression of angiotensin-mediated endothelin production by ACE inhibitors and ATR blockers; CB1 receptor blockers, PKCb inhibitors, nitric oxide donors (glyceryl trinitrate and isosorbide dinitrate), dietary supplements of EPA/DHA and regular physical exercise and control of mental stress.
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PMID:Causation, prevention and reversal of vascular endothelial dysfunction. 1805 38

n-3 and Trans fatty acids are considered to be the important modifiable factors of the metabolic syndrome. The purpose of this study was to test the hypothesis that lower Omega-3 fatty acids and/or higher trans fatty acids of erythrocytes (RBC) are associated with the risk of the metabolic syndrome. Forty-four patients with the metabolic syndrome, defined by three or more risk factors of the modified Adult Treatment Panel III criteria, and eighty-eight age- and sex-matched controls with less than three risk factors were recruited for the study. The mean age was 54.5 (sem 0.8) years and 45 % of subjects were female. Trans fatty acids of RBC were higher in patients than controls (0.82 (sem 0.04) v. 0.73 (sem 0.03) %; P = 0.043), while their Omega-3 indexes, the sum of EPA and DHA in RBC, did not significantly differ (11.78 (sem 0.04) v. 12.39 (sem 0.02) %). Multivariable-adjusted regression analysis showed positive association between trans fatty acid and risk of the metabolic syndrome (OR 7.13; 95 % CI 1.53, 33.27; P = 0.013). Fasting serum insulin (7.9 (sem 0.7) v. 4.9 (sem 0.3) muU/ml; P < 0.001) and high sensitivity C-reactive protein (18 (sem 3) v. 11 (sem 17) mg/l; P = 0.042) were also higher in patients than controls. There were significant positive relationships between trans fatty acids and waist circumference, and between trans fatty acids and BMI. The results suggested that RBC trans fatty acids might be a predictor of increased risk for the metabolic syndrome, but n-3 fatty acids were not in this population.
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PMID:n-3 Polyunsaturated fatty acids and trans fatty acids in patients with the metabolic syndrome: a case-control study in Korea. 1830 91

Hypertriglyceridemia, regarded as one of the independent clinical markers of metabolic syndrome, is a frequently observed disorder that has been shown to be common in the Arab region. Epidemiologic and clinical trials demonstrated that omega-3 fatty acids have the potential to reduce the incidence of cardiovascular disease (CVD); one of the mechanisms by which this effect is achieved is through reducing plasma triglyceride levels. There is strong scientific evidence from human trials that omega-3 fatty acids from either fish or fish oil supplements significantly reduce blood triglyceride levels and these benefits appear to be dose-dependent. The active ingredients of fish oils include the long chain fatty acids EPA and DHA. The ideal amount of omega-3 fatty acid that should be incorporated into the diet without provoking detrimental effects on other lipid components such as decreasing HDL-C and/or increasing LDL-C has not yet been elucidated. Presently, a prescription form of omega-3 fatty acid has been approved by the United States Food and Drug Administration (USFDA) as an adjunct to the diet for the treatment of very high triglyceride levels (> or = 500 mg/dl) in adults. Patients with hypertriglyceridemia have been shown to respond well to the use of omega-3 fatty acids even when used in conjunction with statins where greater improvements in the lipid profile were found as compared to treatment with statins alone. A determinant of the responsiveness to fish oil could be attributed to the ApoE genotype of individuals.
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PMID:Fish oil and the management of hypertriglyceridemia. 1932 19

The insufficient or inappropriate supply of PUFA OMEGA-3 (esp. docosahexaenoic and eicosa pentaenoic acid DHA and EPA) can be suggested to be a common factor of the four metabolic syndrome's clinical manifestations. DHA can be considered as one of the most important element of the membrane. The protective and beneficial effects of DHA (and EPA) result from the dynamic qualities of its molecular structure as well as from its recently detected effects on the genetic expression of several cytokines, enzymes etc. Dietary supplementation of DHA improves all clinical symptoms and laboratory biochemical markers of the metabolic syndrome. Together with that, depletion of DHA was found in diabetes and in several cardiovascular diseases. Also the developmental aspect and approach supports our view. With high probability DHA represents one of the connecting components of the development of metabolic syndrome's clinical manifestations. Metabolic syndrome could be therefore interpreted as an insufficient function of the cellular membrane.
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PMID:Metabolic syndrome (does it have a common denominator?). 1954 90

Adipose tissue has a key role in the development of metabolic syndrome (MS), which includes obesity, type 2 diabetes, dyslipidaemia, hypertension and other disorders. Systemic insulin resistance represents a major factor contributing to the development of MS in obesity. The resistance is precipitated by impaired adipose tissue glucose and lipid metabolism, linked to a low-grade inflammation of adipose tissue and secretion of pro-inflammatory adipokines. Development of MS could be delayed by lifestyle modifications, while both dietary and pharmacological interventions are required for the successful therapy of MS. The n-3 long-chain (LC) PUFA, EPA and DHA, which are abundant in marine fish, act as hypolipidaemic factors, reduce cardiac events and decrease the progression of atherosclerosis. Thus, n-3 LC PUFA represent healthy constituents of diets for patients with MS. In rodents n-3 LC PUFA prevent the development of obesity and impaired glucose tolerance. The effects of n-3 LC PUFA are mediated transcriptionally by AMP-activated protein kinase and by other mechanisms. n-3 LC PUFA activate a metabolic switch toward lipid catabolism and suppression of lipogenesis, i.e. in the liver, adipose tissue and small intestine. This metabolic switch improves dyslipidaemia and reduces ectopic deposition of lipids, resulting in improved insulin signalling. Despite a relatively low accumulation of n-3 LC PUFA in adipose tissue lipids, adipose tissue is specifically linked to the beneficial effects of n-3 LC PUFA, as indicated by (1) the prevention of adipose tissue hyperplasia and hypertrophy, (2) the induction of mitochondrial biogenesis in adipocytes, (3) the induction of adiponectin and (4) the amelioration of adipose tissue inflammation by n-3 LC PUFA.
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PMID:n-3 PUFA: bioavailability and modulation of adipose tissue function. 1969 99

Postprandial lipemia is associated with elevated risk of cardiovascular disease. Very little data exists regarding postprandial response in subjects with metabolic syndrome (MetS). The current study was conducted within the LIPGENE EU Integrated Project. Patients were randomized to one of the four isocaloric fatty meals (Oral Fat Tolerance Tests, OFTT): (A) high-fat, saturated fatty acid (SFA)-rich (HFSA), (B) high-fat, monounsaturated fatty acid (MUFA)-rich (HFMUFA), (C) low-fat, high-complex carbohydrate with 1.24 g high oleic sunflower oil supplement (LFHCC) and (D) low-fat high-complex carbohydrate with 1.24 g long chain n-3 poly-unsaturated fatty acid (LC n-3 PUFA) supplement (LFHCCn-3). The total and incremental areas under the curve (tAUC and iAUC) of plasma lipid and lipoprotein, Ischemia Modified Albumin (IMA) and LDL density were examined in patients with MetS to define effect of OFTT. All types of OFTT transiently increased plasma triglyceride and LDL density (LDLdens). It was paralleled by temporal decrease in total cholesterol (TC), LDL cholesterol (LDL-C), and HDL cholesterol (HDL-C). This last effect was partly alleviated in LFHCCn-3 test. A reversible increase of IMA was statistically significant only in the course of HSFA and HMUFA tests. EPA and DHA supplement in combined high complex-carbohydrate meal may attenuate adverse effect of tested meal on LDL particle profile and plasma ischemia modified albumin. No expected associations between measures of central adiposity (waist, WHR), adipose tissue insulin resistance (Adipo-IR), and postprandial responses of TG, TC, LDL-C, HDL-C, LDLdens and IMA/Alb ratio were found in subgroup analysis.
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PMID:Lipoprotein profile, plasma ischemia modified albumin and LDL density change in the course of postprandial lipemia. Insights from the LIPGENE study. 2023 37

Obesity leads to several chronic morbidities including type 2 diabetes, dyslipidaemia, atherosclerosis and hypertension, which are major components of the metabolic syndrome. White adipose tissue (WAT) metabolism and WAT-derived factors (fatty acids and adipokines) play an important role in the development of these metabolic disturbances. In fact, dysregulated adipokine secretion from the expanded WAT of obese individuals contributes to the development of systemic low-grade inflammation, insulin resistance and metabolic syndrome. The n-3 PUFA EPA and DHA have been widely reported to have protective effects in a range of chronic inflammatory conditions including obesity. In fact, n-3 PUFA have been shown to ameliorate low-grade inflammation in adipose tissue associated with obesity and up-regulate mitochondrial biogenesis and induce beta-oxidation in WAT in mice. Moreover, the ability of n-3 PUFA to regulate adipokine gene expression and secretion has been observed both in vitro and in vivo in rodents and human subjects. The present article reviews: (1) the physiological role of adiponectin, leptin and pre-B cell colony-enhancer factor/visfatin, three adipokines with immune-modulatory properties involved in the regulation of metabolism and insulin sensitivity and (2) the actions of n-3 PUFA on these adipokines focusing on the underlying mechanisms and the potential relationship with the beneficial effects of these fatty acids on obesity-associated metabolic disorders. It can be concluded that the ability of n-3 PUFA to improve obesity and insulin resistance conditions partially results from the modulation of WAT metabolism and the secretion of bioactive adipokines including leptin, adiponectin and visfatin.
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PMID:Regulation of adipokine secretion by n-3 fatty acids. 2054 Aug 25


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