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 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The "metabolic syndrome" (MetS) is a clustering of components that reflect overnutrition, sedentary lifestyles, and resultant excess adiposity. The MetS includes the clustering of abdominal obesity, insulin resistance, dyslipidemia, and elevated blood pressure and is associated with other comorbidities including the prothrombotic state, proinflammatory state, nonalcoholic fatty liver disease, and reproductive disorders. Because the MetS is a cluster of different conditions, and not a single disease, the development of multiple concurrent definitions has resulted. The prevalence of the MetS is increasing to epidemic proportions not only in the United States and the remainder of the urbanized world but also in developing nations. Most studies show that the MetS is associated with an approximate doubling of cardiovascular disease risk and a 5-fold increased risk for incident type 2 diabetes mellitus. Although it is unclear whether there is a unifying pathophysiological mechanism resulting in the MetS, abdominal adiposity and insulin resistance appear to be central to the MetS and its individual components. Lifestyle modification and weight loss should, therefore, be at the core of treating or preventing the MetS and its components. In addition, there is a general consensus that other cardiac risk factors should be aggressively managed in individuals with the MetS. Finally, in 2008 the MetS is an evolving concept that continues to be data driven and evidence based with revisions forthcoming.
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PMID:The metabolic syndrome. 1897 85

In response to stress, some people lose while others gain weight. This is believed to be due to either increased beta-adrenergic activation, the body's main fat-burning mechanism, or increased intake of sugar- and fat-rich "comfort foods." A high-fat, high-sugar (HFS) diet alone, however, cannot account for the epidemic of obesity, and chronic stress alone tends to lower adiposity in mice. Here we discuss how chronic stress, when combined with an HFS diet, leads to abdominal obesity by releasing a sympathetic neurotransmitter, neuropeptide Y (NPY), directly into the adipose tissue. In vitro, when "stressed" with dexamethasone, sympathetic neurons shift toward expressing more NPY, which stimulates endothelial cell (angiogenesis) and preadipocyte proliferation, differentiation, and lipid-filling (adipogenesis) by activating the same NPY-Y2 receptors (Y2Rs). In vivo, chronic stress, consisting of cold water or aggression in HFS-fed mice, stimulates the release of NPY and the expression of Y2Rs in visceral fat, increasing its growth by 50% in 2 weeks. After 3 months, this results in metabolic syndrome-like symptoms with abdominal obesity, inflammation, hyperlipidemia, hyperinsulinemia, glucose intolerance, hepatic steatosis, and hypertension. Remarkably, local intra-fat Y2R inhibition pharmacologically or via adenoviral Y2R knock-down reverses or prevents fat accumulation and metabolic complications. These studies demonstrated for the first time that chronic stress, via the NPY-Y2R pathway, amplifies and accelerates diet-induced obesity and the metabolic syndrome. Our findings also suggest the use of local administration of Y2R antagonists for treatment of obesity and NPY-Y2 agonists for fat augmentation in other clinical applications.
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PMID:Chronic stress, combined with a high-fat/high-sugar diet, shifts sympathetic signaling toward neuropeptide Y and leads to obesity and the metabolic syndrome. 1912 Jan 15

Endocannabinoids are endogenous bioactive lipid mediators present both in the brain and various peripheral tissues, which exert their biological effects via interaction with specific G-protein-coupled cannabinoid receptors, the CB(1) and CB(2). Pathological overactivation of the endocannabinoid system (ECS) in various forms of shock and heart failure may contribute to the underlying pathology and cardiodepressive state by the activation of the cardiovascular CB(1) receptors. Furthermore, tonic activation of CB(1) receptors by endocannabinoids has also been implicated in the development of various cardiovascular risk factors in obesity/metabolic syndrome and diabetes, such as plasma lipid alterations, abdominal obesity, hepatic steatosis, inflammation, and insulin and leptin resistance. In contrast, activation of CB(2) receptors in immune cells exerts various immunomodulatory effects, and the CB(2) receptors in endothelial and inflammatory cells appear to limit the endothelial inflammatory response, chemotaxis, and inflammatory cell adhesion and activation in atherosclerosis and reperfusion injury. Here, we will overview the cardiovascular actions of endocannabinoids and the growing body of evidence implicating the dysregulation of the ECS in a variety of cardiovascular diseases. We will also discuss the therapeutic potential of the modulation of the ECS by selective agonists/antagonists in various cardiovascular disorders associated with inflammation and tissue injury, ranging from myocardial infarction and heart failure to atherosclerosis and cardiometabolic disorders.
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PMID:The emerging role of the endocannabinoid system in cardiovascular disease. 1935 46

We evaluated the prevalence and the risk factors for gallstone disease in patients with chronic hepatitis C infection. We investigated 453 consecutively admitted patients with chronic infection with hepatitis C virus (HCV) (cirrhosis excluded) and 879 patients without liver disease (October 2006-April 2007). Gallstone disease was diagnosed if gallstones were present at ultrasonography or if there had been a previous cholecystectomy. Variables evaluated were age, gender, gallstone heredity, body mass index, waist circumference, parity, serum lipids, fatty liver, arterial hypertension, diabetes mellitus and metabolic syndrome (International Diabetes Federation criteria). Informed consent was obtained from all patients. We found that 88 of 453 (19%) patients with chronic HCV hepatitis (age 50.1 +/- 11.7 years) and 153 of 879 (17%) controls (age 60.6 +/- 12.6 years) had gallstone disease (GD). Abdominal obesity (OR = 2.108, 95% CI 1.287-3.452) and steatosis (OR = 3.699, 95% CI 2.277-6.008) were risk factors for GD in HCV patients. Gallstone heredity, dyslipidaemia, type 2 diabetes mellitus and metabolic syndrome increased the risk for GD in controls vs HCV patients. Our study shows that even HCV patients with chronic hepatitis but not cirrhosis have an increased prevalence of gallstones. Compared with controls, gallstones are present in HCV patients at a younger age and are associated with central obesity and liver steatosis, but not with gallstone heredity, dyslipidaemia, diabetes mellitus or metabolic syndrome. Although we could not establish a temporal relationship, the association between HCV infection and gall stone disease is real and appears to be causally linked, at least in predisposed individuals (obese and with liver steatosis).
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PMID:Hepatitis C virus infection is a risk factor for gallstone disease: a prospective hospital-based study of patients with chronic viral C hepatitis. 1948 79

Childhood obesity continues to escalate despite considerable efforts to reverse the current trends. Childhood obesity is a leading public health concern because overweight-obese youth suffer from comorbidities such as type 2 diabetes mellitus, nonalcoholic fatty liver disease, metabolic syndrome, and cardiovascular disease, conditions once considered limited to adults. This increasing prevalence of chronic health conditions in youth closely parallels the dramatic increase in obesity, in particular abdominal adiposity, in youth. Although mounting evidence in adults demonstrates the benefits of regular physical activity as a treatment strategy for abdominal obesity, the independent role of regular physical activity alone (e.g., without calorie restriction) on abdominal obesity, and in particular visceral fat, is largely unclear in youth. There is some evidence to suggest that, independent of sedentary activity levels (e.g., television watching or playing video games), engaging in higher-intensity physical activity is associated with a lower waist circumference and less visceral fat. Several randomized controlled studies have shown that aerobic types of exercise are protective against age-related increases in visceral adiposity in growing children and adolescents. However, evidence regarding the effect of resistance training alone as a strategy for the treatment of abdominal obesity is lacking and warrants further investigation.
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PMID:Physical activity and abdominal obesity in youth. 1976 90

Young adults with abdominal obesity are liable to have subclinical atherosclerosis that may contribute to an increased risk of cardiovascular disease later in life. This study aims to evaluate subclinical atherosclerosis and its possible correlation with some inflammatory and biochemical markers in Egyptian young adult males with abdominal obesity. The study includes 50 young adult males (age range: 19-29 years) divided into two groups. Group 1 comprises 20 non-obese subjects (controls). Group 2 comprises 30 apparently healthy obese subjects. Carotid intima media thickness (carotid-IMT) was estimated using B-mode ultrasonography of the common carotid arteries, and abdominal ultrasonography was performed to assess the presence of a fatty liver. Laboratory investigations included fasting levels of serum glucose, triglycerides (TG), cholesterol (total [TC], high-density [HDL-cholesterol] and low-density [LDL-cholesterol] lipoprotein fractions), high-sensitivity C-reactive protein (hs-CRP), neopterin, lipoprotein-a (Lp[a]), gamma glutamyl transferase (GGT), aspartate and alanine aminotransferases (AST, ALT), plasma plasminogen and fibrinogen. Results showed that carotid IMT, serum hs-CRP, neopterin, Lp(a), fibrinogen, plasminogen, TC, TG, LDL-cholesterol and liver enzymes were significantly elevated (P<0.001) in the obese group compared to controls. All obese subjects showed evidence of fatty liver. A significant positive correlation was found between carotid-IMT and body mass index, waist circumference, waist/hip ratio, cholesterol, triglycerides, neopterin, hs-CRP AST, ALT and GGT. Elevated serum levels of inflammatory biomarkers and increased ALT, AST and GGT, and non-alcoholic fatty liver disease biomarkers may be useful predictors of subclinical atherosclerosis.
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PMID:Evaluation of some markers of subclinical atherosclerosis in Egyptian young adult males with abdominal obesity. 1983 25

Various anthropometric indices have been proposed for metabolic syndrome. We investigated the clustering of metabolic risk factors other than components of metabolic syndrome and physical activity in subjects with and without metabolic syndrome as defined by different anthropometric indices. The subjects comprised 6141 men and 2137 women who underwent routine health examinations in Tokyo. We compared metabolic risk factors (high low-density lipoprotein cholesterol, hyperuricemia, high gamma-glutamyltransferase, fatty liver) and sedentary history in subjects with and without metabolic syndrome as defined by the American Heart Association by substituting various proposed anthropometric indices of abdominal obesity (waist circumference >or=85, >or=90, or >or=102 cm for men and >or=90, >or=80, or >or=88 cm for women; waist-to-height ratio >or=0.5 for both men and women). Irrespective of the anthropometric index or sex, the age-adjusted odds ratios for risk factors and sedentary history were all significantly greater in subjects with metabolic syndrome (men and women: 1.26 approximately 1.35 and 2.06 approximately 2.63 for high low-density lipoprotein cholesterol, 2.36 approximately 2.60 and 3.88 approximately 7.20 for hyperuricemia, 2.54 approximately 3.02 and 2.92 approximately 4.05 for high gamma-glutamyltransferase, 4.42 approximately 4.87 and 9.43 approximately 12.27 for fatty liver, and 1.37 approximately 1.50 and 1.43 approximately 1.72 for sedentary history). Findings still persisted in those not receiving medication for diabetes mellitus or coronary heart disease. Therefore, attention should be paid to other metabolic risk factors in subjects with metabolic syndrome, irrespective of the anthropometric index or sex. Further study is also needed to clarify the most appropriate definition of metabolic syndrome so as to include the spectrum of risk factors that best represents the future risk of cardiovascular and other diseases.
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PMID:Clustering of other metabolic risk factors in subjects with metabolic syndrome. 1991 45

Mean platelet volume (MPV) is an indicator of platelet activation. Platelet activation and aggregation are central processes in the pathophysiology of coronary heart disease. Non-alcoholic fatty liver disease (NAFLD) is present up to one-third of the general population and the majority of patients with cardio-metabolic risk factors such as abdominal obesity, type 2 diabetes and other components of the metabolic syndrome (MS). The aim of the current study was to investigate the MPV in patients who had NAFLD. MPV values of the patients with NAFLD and of the patients without fatty liver disease were compared. NAFLD patients had significantly higher body mass index compared to the control cases. Among biochemical variables, fasting plasma glucose and triglyceride were significantly higher in the NAFLD group. NAFLD cases also had lower platelet count and higher MPV (10.43 +/- 1.14 vs. 9.09 +/- 1.25; p < 0.001, respectively). MPV was positively correlated with AST (r: 0.186, p < 0.042), ALT level (r: 0.279; p 0.002) and the presence of NAFLD (0.492; p < 0.001) but negatively correlated with platelet number (r: -0.26; p 0.004) and creatinine (r: -0.255; p 0.005). In logistic regression analysis (age, gender, NAFLD, body mass index, high-density lipid (HDL) cholesterol, systolic and diastolic blood pressure, triglyceride and fasting plasma glucose were used as covariates) only NAFLD was found to be the independent predictor of MPV (Odds Ratio (OR) 21.98) [95% confidence interval (CI): 2.404-201.048; p: 0.006]. We have shown for the first time in the literature that, patients with NAFLD have higher MPV. It may have prognostic value in NAFLD patients indicating a possible cardiovascular disease (CVD) risk increase.
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PMID:Mean platelet volume in patients with non-alcoholic fatty liver disease. 2114 6

Abdominal obesity represents a public health concern because its prevalence is reaching epidemic proportions worldwide, and it is associated with an increased risk of cardiovascular morbidity and mortality and other pathological conditions. A large body of evidence suggests that abdominal obesity is associated with a prothrombotic tendency, which may, at least in part, contribute to the increased risk of atherothrombosis in these individuals. This review briefly summarizes the evidence of direct and indirect effects of the accumulation of excess lipid in visceral adipose tissue on coagulation and fibrinolysis. In addition, this article critically appraises the rapidly expanding body of experimental and clinical data that support a potential direct contribution for the accumulation of excess lipid in the liver (i.e., nonalcoholic fatty liver disease, a very frequent pathological condition in subjects with abdominal obesity) in the pathogenesis of the obesity-induced disorders of coagulation and fibrinolysis.
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PMID:Disorders of coagulation and hemostasis in abdominal obesity: emerging role of fatty liver. 2039 Dec 95

Obesity and related diseases are an important and growing health concern in the United States and around the world. Soft drinks and other sugar-sweetened beverages are now the primary sources of added sugars in Americans' diets. The metabolic syndrome is a cluster of common pathologies, including abdominal obesity linked to an excess of visceral fat, fatty liver, insulin resistance, hyperinsulinemia, dyslipidemia, and hypertension. Trends in all of these alterations are related to the consumption of dietary fructose and the introduction of high-fructose corn syrup (HFCS) as a sweetener in soft drinks and other foods. Experimental and clinical evidence suggests a progressive association between HFCS consumption, obesity, and the other injury processes. However, experimental HFCS consumption seems to produce some of the changes associated with metabolic syndrome even without increasing the body weight. Metabolic damage associated with HFCS probably is not limited to obesity-pathway mechanisms.
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PMID:The role of high-fructose corn syrup in metabolic syndrome and hypertension. 2042 37


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