Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The potential role of anti-inflammatory cytokines in human obesity is unknown. We tested the hypothesis that low serum IL-10 concentrations associate with the metabolic syndrome in obese women. Compared with 50 matched nonobese women, the prevalence of the metabolic syndrome (>/=3 of the following abnormalities: waist circumference, >88 cm; triglycerides, >1.69 mmol/liter; high density lipoprotein cholesterol, <1.29 mmol/liter; blood pressure, >130/85 mm Hg; glucose, >6.1 mmol/liter) was higher in 50 obese women (52% vs. 16%; P < 0.01). As a group, obese women had higher circulating levels of IL-6, C-reactive protein, and IL-10 than nonobese women. In both obese and nonobese women, IL-10 levels were lower in those with than in women without the metabolic syndrome: obese, 1.3 (0.7/2.1) pg/ml vs. 4.5 (4.3/7.4) pg/ml (median and quartiles; P < 0.01); and nonobese, 0.9 (0.7/1.3) pg/ml vs. 1.3 (0.9/3.3) pg/ml (P < 0.05). After 12 months of a lifestyle program, body weight decreased by 10.9 +/- 1.7 kg and was associated with a significant decrement of IL-6, C-reactive protein, and IL-10 levels; the decrease in IL-10 levels was confined to obese women without the metabolic syndrome. These results show that circulating levels of the anti-inflammatory cytokine IL-10 are elevated in obese women and that low IL-10 levels are associated with the metabolic syndrome.
 ...
PMID:Association of low interleukin-10 levels with the metabolic syndrome in obese women. 1262 85

Cardiovascular diseases (CVD) remain the major cause of death in postmenopausal women. Before menopause, women are relatively protected from ischemic heart disease and thromboembolism by their circulating estrogens, but this protection is lost after menopause. Following menopause, adverse lipid changes occur and the levels of several coagulation factor increase. One of the major predisposing factors for CVD is the metabolic syndrome, including myriad risk biomarkers: abdominal girth, blood pressure, fasting glucose, triglycerides, lipids. In many ways, the metabolic syndrome is a precursor to the development of abnormalities of insulin action and diabetes. In parallel, there are effects upon blood coagulation and fibrinolysis. Common preventive therapies require rigorous evaluation. Hormone replacement therapy (HRT) has not produced the expected reduction in CVD and the ideal HRT is probably unobtainable. For long-term HRT users, the risk of thromboembolism needs to be weighed against probable benefits. With respect to the effects of HRT, oral estrogen is associated with elevation in C-reactive protein and varied effects on IL-6, but transdermal estradiol has no significant effect on these parameters. Despite the varied effects of HRT on inflammatory biomarkers, there is no definitive evidence that change in these markers results in modification of cardiovascular risk.
 ...
PMID:[The metabolic syndrome in postmenopausal women. Clinical implications]. 1472 60

Adiponectin is a novel adipocytokine negatively correlated with parameters of the metabolic syndrome, such as body mass index (BMI), body fat mass (BFM), and circulating insulin levels. Furthermore, metabolic actions directly on the liver have been described. The aim of the present study was to characterize circulating adiponectin levels, hepatic turnover, and the association of adiponectin with key parameters of hepatic as well as systemic metabolism in cirrhosis, a catabolic disease. Circulating adiponectin levels and hepatic turnover were investigated in 20 patients with advanced cirrhosis. Hepatic hemodynamics [portal pressure, liver blood flow, hepatic vascular resistance, indocyanine green (ICG) half-life], body composition, resting energy expenditure, hepatic free fatty acids (FFA) and glucose turnover, and circulating levels of hormones (catecholamines, insulin, glucagon) and proinflammatory cytokines (IL-1beta, TNF-alpha, IL-6) were also assessed. Circulating adiponectin increased dependently on the clinical stage in cirrhosis compared with controls (15.2 +/- 1.7 vs. 8.2 +/- 1.1 microg/ml, respectively, P < 0.01), whereas hepatic extraction decreased. Adiponectin was negatively correlated with parameters of hepatic protein synthesis (prothrombin time: r = -0.62, P = 0.003; albumin: r = -0.72, P < 0.001) but not with transaminases or parameters of lipid metabolism. In addition, circulating adiponectin increased with portal pressure (r = 0.67, P = 0.003), hepatic vascular resistance (r = 0.60, P = 0.008), and effective hepatic blood flow (ICG half-life: r = 0.69, P = 0.001). Adiponectin in cirrhosis was not correlated with BMI, BFM, parameters of energy metabolism, insulin levels, hepatic FFA and glucose turnover, and circulating proinflammatory cytokines. These results demonstrate that 1) adiponectin plasma levels in cirrhosis are significantly elevated, 2) the liver is a major source of adiponectin extraction, and 3) adiponectin levels in cirrhosis do not correlate with parameters of body composition or metabolism but exclusively with reduced liver function and altered hepatic hemodynamics.
 ...
PMID:Elevated circulating adiponectin levels in liver cirrhosis are associated with reduced liver function and altered hepatic hemodynamics. 1501 Mar 38

The level of interleukin-18 (IL-18) is elevated in patients with HIV infection as well as in people with insulin resistance (IR). As HIV-associated lipodystrophy (LD) shares metabolic characteristics with the metabolic syndrome, it was hypothesized that IL-18 would be elevated in patients with LD. Two groups of HIV-infected men with LD, one with fat accumulation (mixed group) (n = 12) and one without fat accumulation (lipoatrophic group) (n = 15) were included. Controls were HIV-positive men without LD (n = 15) and HIV-negative, age-matched men (n = 12). The levels of plasma IL-18 were elevated in all 3 HIV groups compared with HIV-negative controls (P <0.01). In the HIV groups the lipoatrophic group had the highest IL-18, followed by the mixed group and the HIV-positive controls. Only the differences between the lipoatrophic group and the HIV-positive controls were significant (P <0.01). Plasma IL-18 correlated with tumor necrosis factor-alpha (P <0.05), but not IL-6, adiponectin, or HOMA-IR (homeostasis model of insulin resistance). In contrast to the HIV-negative controls, IL-18 did not correlate with total or low-density cholesterol in either of the HIV groups. An inverse correlation was observed between IL-18 and limb fat (P <0.05). In conclusion, the level of IL-18 is elevated in patients with LD and closely linked to limb atrophy, whereas it is not associated with cholesterol or IR.
 ...
PMID:High plasma level of interleukin-18 in HIV-infected subjects with lipodystrophy. 1509 1

Insulin resistance is an important component of the metabolic syndrome associated with obesity. Early-stage insulin-resistance and related mild glucose intolerance may be compensated by increased insulin secretion. When combined with impaired insulin secretion, insulin resistance plays an important role in type 2 diabetes (1). Insulin-resistance is also associated with a variety of pathological conditions, including trauma, infection, and cancer. Obesity and type 2 diabetes are the most common metabolic diseases in Western societies, together affecting as much as half of the adult population (2). The prevalence of these conditions is not only high, but continues to increase. We have only recently come to appreciate the role of fat, especially visceral fat, as an endocrine organ. Visceral fat is the source of a number of substances which might play a role in the development of insulin resistance. Among the latter are tumor necrosis factor-alpha (TNF-alpha), adiponectin, IL-6, resistin and free fatty acids. This review will discuss the regulation of insulin responses by TNF-alpha and evidence supporting the hypothesis that over expression of TNF-alpha plays a role in the pathophysiology of insulin resistance.
 ...
PMID:The role of TNF-alpha in insulin resistance. 1514 98

Long-term observation studies on metabolic syndrome have disclosed that accumulation of clinical features in the syndrome indicated poor prognosis in the subjects. High sensitivity CRP(hs CRP) is generally increased in the obese subjects due to increased TNF alpha and IL-6 in adipose tissue. Hs CRP is also elevated in hypertensive and diabetic subjects. Hs CRP is increased in the subjects with low HDL-cholesterol and high triglyceride. The West of Scotland Coronary Prevention Study indicated that metabolic syndrome with or without hs CRP more than 3 mg/l predicted definite differences in prognosis for future cardiac outcomes.
 ...
PMID:[Enhanced prognostic information by determining hs CRP on metabolic syndrome]. 1520 52

Risk of coronary heart disease has been related to insulin resistance, but the mechanism for this is incompletely understood. Variables attributed to insulin resistance are associated with low-grade inflammation. A case-control study was performed of 469 male myocardial infarction (MI) survivors aged < 60 years and 575 control subjects recruited from centers in northern and southern Europe. Principal factor analysis was used to explore correlations between insulin resistance and inflammatory variables. Three factors resulted: (a) "Metabolic Syndrome" (insulin/proinsulin/ triglyceride/body mass index [BMI]); (b) "Inflammation" (fibrinogen/C-reactive protein [CRP]/interleukin-6 [IL-6]); and (c) "Blood Pressure" (systolic and diastolic blood pressure). The "Metabolic Syndrome" factor was related to the "Inflammation" factor (largely independently of obesity), the "Blood Pressure" factor, smoking, and south location (all P < or = .0002). There were significant relationships between all 3 factors and case status (P < or = .0002). Markers of low-grade inflammation are strongly related to metabolic syndrome variables independently of obesity. This raises the possibility that links between insulin resistance and cardiovascular disease could, in part, represent common consequences of low-grade inflammation.
 ...
PMID:Low-grade inflammation may play a role in the etiology of the metabolic syndrome in patients with coronary heart disease: the HIFMECH study. 1525 76

White adipose tissue is now recognised to be a multifunctional organ; in addition to the central role of lipid storage, it has a major endocrine function secreting several hormones, notably leptin and adiponectin, and a diverse range of other protein factors. These various protein signals have been given the collective name 'adipocytokines' or 'adipokines'. However, since most are neither 'cytokines' nor 'cytokine-like', it is recommended that the term 'adipokine' be universally adopted to describe a protein that is secreted from (and synthesised by) adipocytes. It is suggested that the term is restricted to proteins secreted from adipocytes, excluding signals released only by the other cell types (such as macrophages) in adipose tissue. The adipokinome (which together with lipid moieties released, such as fatty acids and prostaglandins, constitute the secretome of fat cells) includes proteins involved in lipid metabolism, insulin sensitivity, the alternative complement system, vascular haemostasis, blood pressure regulation and angiogenesis, as well as the regulation of energy balance. In addition, there is a growing list of adipokines involved in inflammation (TNFalpha, IL-1beta, IL-6, IL-8, IL-10, transforming growth factor-beta, nerve growth factor) and the acute-phase response (plasminogen activator inhibitor-1, haptoglobin, serum amyloid A). Production of these proteins by adipose tissue is increased in obesity, and raised circulating levels of several acute-phase proteins and inflammatory cytokines has led to the view that the obese are characterised by a state of chronic low-grade inflammation, and that this links causally to insulin resistance and the metabolic syndrome. It is, however, unclear as to the extent to which adipose tissue contributes quantitatively to the elevated circulating levels of these factors in obesity and whether there is a generalised or local state of inflammation. The parsimonious view is that the increased production of inflammatory cytokines and acute-phase proteins by adipose tissue in obesity relates primarily to localised events within the expanding fat depots. It is suggested that these events reflect hypoxia in parts of the growing adipose tissue mass in advance of angiogenesis, and involve the key controller of the cellular response to hypoxia, the transcription factor hypoxia inducible factor-1.
 ...
PMID:Adipokines: inflammation and the pleiotropic role of white adipose tissue. 1546 38

Elevated blood concentrations of IL-6 have been shown to predict type 2 diabetes. Because the impact of IL-6 gene polymorphisms on diabetes status, parameters of the metabolic syndrome, and low-grade systemic inflammation has not been analyzed in a population-based study, we investigated the association of the IL-6 single nucleotide polymorphisms C-174G and A-598G on these parameters in 704 elderly participants of the Kooperative Gesundheitsforschung im Raum Augsburg/Cooperative Research in the Region of Augsburg (KORA) Survey 2000. Both -174G and -598G alleles were significantly associated with type 2 diabetes (-174G: odds ratio = 1.51, 95% confidence interval = 1.11-2.07, P = 0.0096; -598G: odds ratio = 1.56, 95% confidence interval = 1.13-2.15, P = 0.0069) but not with impaired glucose tolerance. In subgroup analyses, the association reached statistical significance in men and in leaner subjects (body mass index <or= 28.7 kg/m(2), i.e. study median) but not in women or more obese persons. Circulating IL-6 levels were not associated with the IL-6 polymorphisms, but significantly elevated levels of the chemokine monocyte chemoattractant protein-1/CC chemokine ligand 2 in carriers of the protective genotypes indicated an indirect effect of these single nucleotide polymorphisms on the innate immune system. Our findings confirm that immune gene polymorphisms can be considered as independent risk factors in the etiology of type 2 diabetes and suggest that their contribution may be indirect, by influencing the levels of other immune mediators like monocyte chemoattractant protein-1.
 ...
PMID:Significant association of the interleukin-6 gene polymorphisms C-174G and A-598G with type 2 diabetes. 1547 5

The purpose of this study was to investigate whether aerobic fitness, body composition, body fat distribution, and inflammation are different in obese postmenopausal women with and without the metabolic syndrome (MS), and whether the severity of MS is associated with these characteristics. Fifty-eight women (age, 59 +/- 1 yr; body mass index, 33.0 +/- 0.6 kg/m2)completed testing of maximal aerobic capacity, body composition (fat mass, lean mass, and percent body fat), body fat distribution (sc and visceral fat areas, and regional adipocyte sizes), and inflammation (C-reactive protein, IL-6, and TNF-alpha,and their soluble receptors). Lean mass (44.4 +/- 0.9 vs. 41.2 +/- 0.9 kg; P < 0.05), visceral fat area (180 +/- 10 vs. 135 +/- 7 cm2; P <0.001), and plasma soluble TNF receptor 1 (sTNFR1; 860 +/- 25 vs. 765 +/- 42 pg/ml; P < 0.05) were higher in women with the MS(n = 27) than in those without the MS (n = 31). The number of MS components was directly related to weight, body mass index, fat mass, lean mass, visceral fat area, and plasma sT-NFR1. We conclude that obese older women with the MS are characterized by high lean mass, high visceral fat, and elevated sTNFR1, and the severity of the MS is associated with body composition, visceral adiposity, and inflammation.
 ...
PMID:The metabolic syndrome in obese postmenopausal women: relationship to body composition, visceral fat, and inflammation. 1548 17


1 2 3 4 5 6 7 8 9 10 Next >>