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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atherogenic low density lipoproteins (LDL) consist of subfractions of particles with different dimensions, density, proportion of various lipid components, affinity to apo B/E receptors, susceptibility to oxidation, and other properties. As a rule spectrum of LDL particles has one predominant central peak and several (up to 6) additional peaks containing particles which are smaller or larger than particles of the main peak. There are also smaller and bigger particles within the main peak itself. In normolipidemia average diameter of particles of the predominant main peak exceeds 25.5 hm (profile A), in combined hyperlipidemia main peak consists of smaller (<25.5 hm) particles (profile B). It has been shown in many studies that because of several characteristics (lower affinity to apo B/E receptors, prolonged presence in blood stream, susceptibility to oxidation and uncontrolled entrapment by macrophages) small dense LDL particles play significant role in atherogenesis. The authors of this review have demonstrated that in subjects with abdominal obesity and concomitant metabolic risk factors in postprandial period after standard meal LDL spectrum shifts towards small particles and this shift persists during 6 hours after meal. An apparently atherogenic subfraction of large cholesterol ester loaded particles is also described in this paper.
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PMID:[Small dense low density lipoprotein particles: mechanisms of formation, atherogenic properties, possibilities of modification of their content in blood plasma]. 1623 81

Recent studies suggest that adipose tissue hormones ("adipokines") are involved in the pathogenesis of various complications of obesity, including hyperlipidemia, diabetes mellitus, arterial hypertension, atherosclerosis, and heart failure. Apelin and visfatin are two recently described adipokines, although they are also synthesized outside adipose tissue. Apelin exists in at least three forms, consisting of 13, 17, or 36 amino acids, all originating from a common 77-amino-acid precursor. In the cardiovascular system, apelin elicits endothelium-dependent, nitric oxide-mediated vasorelaxation and reduces arterial blood pressure. In addition, apelin demonstrates potent and long-lasting positive inotropic activity which is preserved even in injured myocardium and is not accompanied by myocardial hypertrophy. Apelin synthesis in adipocytes is stimulated by insulin, and plasma apelin level markedly increases in obesity associated with insulin resistance and hyperinsulinemia. In addition to regulating cardiovascular function, apelin inhibits water intake and vasopressin production. Visfatin, previously recognized as a pre-B cell colony-enhancing factor (PBEF), is abundantly expressed in visceral adipose tissue and is upregulated in some, but not all, animal models of obesity. Preliminary studies suggest that plasma visfatin concentration is also increased in humans with abdominal obesity and/or type 2 diabetes mellitus. Visfatin binds to the insulin receptor at a site distinct from insulin and exerts hypoglycemic effect by reducing glucose release from hepatocytes and stimulating glucose utilization in peripheral tissues. Thus, apelin and visfatin are unique among adipose tissue hormones in that they are upregulated in the obese state and both exert primarily beneficial effects.
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PMID:Apelin and visfatin: unique "beneficial" adipokines upregulated in obesity? 1694 Sep 39

In spite of a progressive fall in the incidence of traditional risk factors of cardiovascular morbidity (cigarette smoking, high blood pressure, and hyperlipidemia), there is an upward trend in the prevalence of obesity and chronic kidney disease (CKD). Furthermore, there is a strong correlation between body mass indices and the relative risk of progression of CKD. The close biophysiological interaction between obesity and CKD is evident by a similar occurrence of comorbidities including insulin resistance, hyperlipidermia, endothelial dysfunction, and sleep disorders. Truncal obesity is a primary component of metabolic syndrome; unlike peripheral fat, the visceral adipocytes are more resistant to insulin. In addition, lipolysis results in a release of free fatty acid and TG, whereas hypertriglycedemia is potentiated by uremic activation of fatty acid synthase. Hypertriglycedemia and low HDL cholesterol increase the relative risk of progression of CKD. Furthermore, endothelial inflammation and premature atherosclerosis are promoted by hyperhomocysteinemia and oxidation of LDL, both of which are commonly observed in CKD and obesity. Predominance of oxidative stress in both obesity and azotemia stimulate synthesis of angiotensin II, which in turn increases TGF-B and plasminogen activator inhibitor-1, thereby propagating glomerular fibrosis. Furthermore, local synthesis of angiotensinogen by adipocytes, leptin activation of sympathetic nervous system, and hyperinsulinemia contribute to the development of hypertension in obesity and CKD. In addition, increased renal tubular expression of Na-K-ATPase and a blunted response to natiuretic hormones in obesity promote salt and water retention. Glomerular hyperfiltration from systemic volume load and hypertension results in mesangial cellular proliferation and progressive renal fibrosis. In addition, maternal nutritional deprivation increases the incidence of obesity, hypertension, and diabetes in adulthood. Reduced fetal protein synthesis contributes to oxidative glomerular injury and impairment of renal morphogenesis. Thus, kidneys are poorly equipped to handle physiologic stress that may result from the rapid body growth and programmed metabolic dysfunction later in life. Finally, in order to minimize morbidity of obesity-related kidney disease, preventive strategy must include optimal maternal health care, promotion of healthy nutrition and routine physical exercise, and early detection of CKD.
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PMID:The role of obesity and its bioclinical correlates in the progression of chronic kidney disease. 1704 21

Recent studies have suggested that several systemic conditions--such as obesity, hypertension, hyperlipidemia, and diabetes--are related to periodontitis. The objective of this study was to examine the relationship between periodontitis and 5 components of metabolic syndrome--abdominal obesity, triglyceride level, high-density lipoprotein cholesterol level, blood pressure, and fasting blood sugar level--in 584 Japanese women. In multivariate analyses, persons exhibiting more components of metabolic syndrome had significantly higher odds ratios for a greater pocket depth and clinical attachment loss than did those with no components; the odds ratios for a greater pocket depth and clinical attachment loss of the persons exhibiting 4 or 5 components were 6.6 (95% confidence interval = 2.6-16.4) and 4.2 (95% confidence interval = 1.2-14.8), respectively. These results indicate that metabolic syndrome increases risk of periodontitis, and suggest that people exhibiting several components of metabolic syndrome should be encouraged to undergo a periodontal examination.
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PMID:Relationship of metabolic syndrome to periodontal disease in Japanese women: the Hisayama Study. 1731 61

The metabolic syndrome is a cluster of common pathologies: abdominal obesity linked to an excess of visceral fat, insulin resistance, dyslipidemia and hypertension. This syndrome is occurring at epidemic rates, with dramatic consequences for human health worldwide, and appears to have emerged largely from changes in our diet and reduced physical activity. An important but not well-appreciated dietary change has been the substantial increase in fructose intake, which appears to be an important causative factor in the metabolic syndrome. There is also experimental and clinical evidence that the amount of magnesium in the western diet is insufficient to meet individual needs and that magnesium deficiency may contribute to insulin resistance. In recent years, several studies have been published that implicate subclinical chronic inflammation as an important pathogenic factor in the development of metabolic syndrome. Pro-inflammatory molecules produced by adipose tissue have been implicated in the development of insulin resistance. The present review will discuss experimental evidence showing that the metabolic syndrome, high fructose intake and low magnesium diet may all be linked to the inflammatory response. In many ways, fructose-fed rats display the changes observed in the metabolic syndrome and recent studies indicate that high-fructose feeding is associated with NADPH oxidase and renin-angiotensin activation. The production of reactive oxygen species results in the initiation and development of insulin resistance, hyperlipemia and high blood pressure in this model. In this rat model, a few days of experimental magnesium deficiency produces a clinical inflammatory syndrome characterized by leukocyte and macrophage activation, release of inflammatory cytokines, appearance of the acute phase proteins and excessive production of free radicals. Because magnesium acts as a natural calcium antagonist, the molecular basis for the inflammatory response is probably the result of a modulation of the intracellular calcium concentration. Potential mechanisms include the priming of phagocytic cells, the opening of calcium channels, activation of N-methyl-D-aspartate (NMDA) receptors, the activation of nuclear factor-kappaB (NFkB) and activation of the renin-angiotensin system. Since magnesium deficiency has a pro-inflammatory effect, the expected consequence would be an increased risk of developing insulin resistance when magnesium deficiency is combined with a high-fructose diet. Accordingly, magnesium deficiency combined with a high-fructose diet induces insulin resistance, hypertension, dyslipidemia, endothelial activation and prothrombic changes in combination with the upregulation of markers of inflammation and oxidative stress.
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PMID:High fructose consumption combined with low dietary magnesium intake may increase the incidence of the metabolic syndrome by inducing inflammation. 1740 91

Obesity and overweight, as a part of the metabolic syndrome, are well known risk factors for the development of diabetes, hypertension, coronary heart disease, hyperlipidemia, stroke, sleep apnea syndrome, osteoarthritis and certain forms of cancer. Cardiovascular disease remains the leading killer in industrialized countries, where it accounts for 40% of deaths. Obesity is defined either by increased waist circumference, waist to hip ratio, or body mass index. Obesity results from an interaction of genes and lifestyle. As people in both developed and developing countries eat more and more energy dense food, and have ever less physical activity, the number of overweight and obese people increases to epidemic proportions. Abdominal obesity plays a key role in the pathophysiology of metabolic disorders, is associated with insulin resistance, and predicts the development of type 2 diabetes and subsequent coronary artery disease. In the general population, obesity is associated with an increased mortality, but paradoxically, a positive correlation between body mass index and survival in congestive heart failure has been reported. In secondary prevention, obesity is underrecognized, underdiagnosed and undertreated in persons with cardiovascular diseases. Weight loss and prevention of weight gain have to be considered one of the most important strategies to reduce the incidence of cardiovascular disease. Increased physical activity and appropriate diet are the cornestones of treatment. Considering the high prevalence of overweight and obesity in Croatia, there is urgent necessity to improve the level of knowledge and skills in understanding obesity by health care services, and to implement appropriate professional strategy to achieve the desired lifestyle modifications.
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PMID:[Obesity--a global public health problem]. 1758 71

Parameters of HDL (concentrations of cholesterol, apoprotein A1, and phospholipids and phospholipid composition) determining their functional properties were studied in patients with arterial hypertension in combination with other components of metabolic syndrome (abdominal obesity, hyperlipidemia, and impaired glucose tolerance). Patients with isolated arterial hypertension did not differ from the control group by the concentration of apoprotein A1 and HDL cholesterol, but had lower content of HDL phospholipids and changed phospholipid composition: lower ratio of phosphatidylcholine and higher relative contents of lysophosphatidylcholine, sphingomyelin, and phosphatidylethanolamine. Parameters of HDL in patients with arterial hypertension associated with other components of metabolic syndrome did not differ from those in patients with isolated arterial hypertension. The observed changes in HDL in patients with arterial hypertension alone or in combination with other components of metabolic syndrome can impair functional capacity of HDL in reverse cholesterol transport, which increases the risk of atherosclerosis.
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PMID:Parameters of high-density lipoproteins in patients with arterial hypertension in combination with other components of metabolic syndrome. 1822 52

The aim of the study was to identify incremental values of carotid ultrasound measurements (carotid plaques and stenosis) on the prediction of future coronary revascularization among type 2 diabetic patients. The second objective was to determine the predictive value of the assessment of blood lipids, BMI, abdominal obesity and the ankle-brachial index (ABI). Three hundred and thirty three (333) patients with type 2 diabetes and manifested coronary artery disease were randomly selected in a cohort prospective study. Univariate and multivariate logistic regression analyses were conducted to identify variables predictive of the need for future revascularization: percutaneus coronary interventions (PCI) or coronary bypass surgery (CABG) followed 24 months after the study starting point. The presence of arterial hypertension, hyperlipidemia, physical inactivity, intermittent claudication, the value of systolic pressure, BMI, waist and hip measurement, glycemia and blood lipid fraction (total cholesterol, HDL, LDL, non-HDL, triglycerides) were entered in a model. Ultrasound measurements: carotid IMT, presence of carotid plaques and stenosis, and ABI were also included in the analysis. Based on the univariate and multivariate findings, the presence of internal carotid artery (ICA) stenosis (OR 4,562, 95% CI 1,327-15,687), carotid plaque (OR 1,465, 95% CI 0,829-2,591), and increased waist measurement (OR 1,371, 95% CI 0,757-2,483) were found as significant independent predictors of future PCI. LDL and non HDL cholesterol were found to be factors independently associated with the need for future CABG by univariate analysis, which was not confirmed by multivariate analysis. In conclusion, the current study has provided an identification of predisposing factors for the future need of coronary revascularization among type 2 diabetic patients that permits risk stratification and may facilitate improved patient selection or optimization.
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PMID:Carotid ultrasound, blood lipids and waist determination can predict a future coronary revascularisation in the type 2 diabetic cohort. 1835 84

Risk factors are generally shared between men and women with the major differences being hormonal. Nine modifiable risk factors account for over 90% of the risk of a coronary event in men and women--smoking, hypertension, hyperlipidaemia, diabetes, abdominal obesity, lack of exercise, alcohol excess, reduced intake of fruit and vegetables, and psychosocial issues. Approximately half the decline in deaths from coronary heart disease (CHD), between 1980 and 2000, can be attributed to a reduction in the major risk factors and the other half to the use of evidence-based management. As educational efforts to increase awareness of cardiovascular disease (not cancer) to be the leading cause of death and disability in women are also associated with preventative action, it is important that health-care professionals educate themselves about CHD in women and communicate with women themselves, so that women can come forward for advice and evaluation.
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PMID:Gender differences in cardiovascular disease prevention. 1838 Sep 55

Metabolic syndrome is a combination of metabolic-related health issues such as hypertension, hyperlipidaemia and hyperinsulinaemia that together increase significantly the risk of cardiovascular disease and type 2 diabetes. Its prevalence has dramatically increased over the last several decades throughout the world following that of obesity. Insulin resistance and abdominal obesity are considered its core, while the latter may generate via complex metabolic and biochemical pathways the rest parameters of metabolic syndrome. The current approach of treatment is based on treating the chronic cardiovascular malfunctions but there is increasing interest in approaches to managing abdominal obesity as the underlying cause.
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PMID:Obesity; epiphenomenon or cause of metabolic syndrome? 1847 86


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