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Metabolic syndrome is a clustering of risk factors for cardiovascular disease. The Expert Panel on the Detection, Evaluation, and Treatment on High Blood Cholesterol in Adults (Adult Treatment Panel III) defines the syndrome as three or more of the following criteria 1. Abdominal obesity waist circumference 102 cm in men and 88 cm in women Obesity is a component of metabolic syndrome, but it is not absolutely required to make the diagnosis if other criteria are present. Diagnosis of metabolic syndrome is important to alert the clinician of increased risk of diabetes and cardiovascular disease. The prevalence of US adults having the metabolic syndrome is 22 , and it is even more common among high risk groups such as women with polycystic ovary syndrome with about a third of women affected.
Although PCOS often presents in the early reproductive years, it is now recognized that the consequences of PCOS extend beyond the reproductive axis and the reproductive years. Women with PCOS appear to be at substantial risk of developing diabetes and cardiovascular disease. Several studies indicate that the risk of metabolic syndrome in PCOS is approximately 50 in young adulthood. Metabolic syndrome is a constellation of metabolic risk factors that increase the risk of cardiovascular events 2-fold. For women, these include increased abdominal waist circumference ( 88 cm), elevated triglycerides ( 150 mg dL), reduced HDL ( 130 mm Hg systolic or 85 mm Hg diastolic or drug treatment for hypertension), and elevated fasting glucose ( 100 mg dL).
Increased serum FFA, as a facet of the metabolic syndrome, adversely alters vascular function and constitutes an independent risk factor for coronary disease (Sattar et al., 1998). Experiments on endothelial cells in culture and on rat femoral artery segments in vitro suggest that physiologically relevant concentrations of FFA cause reductions in vasodilator prostacyclin and nitric oxide and reductions in vascular relaxation responsiveness (Davda et al., 1995 Endresen et al., 1994). In lean, insulin-sensitive subjects, manipulations to increase circulating FFA levels to the range observed in insulin-resistant patients (two- to ninefold elevations) impair relaxation to the endothelium-dependent vasodilator methacholine as measured by leg blood flow (Steinberg et al., 1997, 2000). Endogenous FFA correlate well with adverse vascular function in vivo (Steinberg et al., 1996, 1997, 2000). As discussed by these authors, elevated FFA may induce formation of reactive oxygen species which...
Vascular diseases are characterised by conditions that clog or weaken blood vessels. They have been widely investigated as they represent a major cause of death in industrialised countries (Minino et al. 2002 Gianazza and Sironi 2004). Vascular diseases are mainly caused by elevated levels of cholesterol and triglycerides in the blood, hypertension, hyperhomocysteinemia, diabetes and obesity, systemic inflammation and metabolic syndrome, but also a lack of physical activity, cigarette smoking, a high-fat diet, low antioxidant levels and infectious agents. Gender and age may also play a role. Vascular diseases involve many different processes. These include slow processes, such as atherosclerosis that can evolve over decades, and much more rapid events, such as infarction in the heart or the brain.
It is likely that both maternal and placental factors cause dyslipidemia in pre-eclampsia. The insulin resistance syndrome, a cluster of metabolic abnormalities associated with reduced insulin sensitivity, is a strong predisposing factor for cardiovascular disease (Kahn and Flier, 2000 Reaven, 1994). Pre-eclampsia is associated with accentuation of many features of the metabolic syndrome, including insulin resistance, hypertri-glyceridemia, elevated FFA, low HDL cholesterol, hyperuricemia, and abnormalities in the fibrinoly-tic system, usually in the absence of frank diabetes (Kaaja, 1998 Kaaja et al., 1995 Lorentzen et al., 1998 Solomon et al., 1994 Solomon et al., 1999 Sowers et al., 1995 Wolf et al., 2002). Accompanying abnormalities include increased serum concentrations of leptin, C-reactive protein, tumor necrosis factor-a, testosterone, and plasminogen activator-inhibitor-1 (Sattar and Greer, 2002 Wolf etal., 2001).
Being overweight or obese, particularly abdominal obesity 139 , has been linked to an increased CRC risk, especially in men 140 . The mechanism is complex and the effect of being overweight or obese reflects the negative consequences of high energy intake and metabolic changes. Hyperinsulinaemia 141 and high levels of insulin-like growth factor-1 (IGF-1) 142 could contribute to the CRC risk. However, while being overweight and having a higher Body Mass Index may be strongly related to colon cancer, the link appears to be weaker for rectal can
Life (Hubel et a ., 2000 Sattar and Greer, 2002). As mentioned previously, the insulin resistance syndrome is a key factor underlying non-pregnancy cardiovascular disease. The maternal physiologic response to normal pregnancy includes a transient excursion into several aspects of this metabolic syndrome, i.e. insulin resistance, hyper-lipidemia, and an increase in coagulation factors (Herrera et a ., 1988 Hubel et a ., 1998b Martin et a ., 1999 Montes et a ., 1984 Sattar and Greer, 2002). Normal pregnancy also involves upregula-tion of the inflammatory cascade including activation of peripheral white blood cells (Sacks et a ., 1998, 1999). Upregulation of the inflammatory cascade in non-pregnant women is a strong risk factor for adverse cardiovascular events and diabetes (Ross, 1999). Several lines of evidence suggest that pregnancy represents a ''stress test'' of maternal carbohydrate, lipid, and inflammatory pathways, and vascular function (Agatisa et a ., 2004 Barden et a ., 1999...
It is an apparent paradox that obesity is associated with a systemic inflammatory response involving TNF-a, a cytokine that induces cachexia among its other actions. A cluster of clinical features including obesity is variously called the metabolic syndrome, syndrome X or the insulin resistance syndrome (Isomaa, 2003). Components of the syndrome include insulin resistance, impaired glucose tolerance or overt diabetes,
Waist circumference has been found to be an independent risk factor for disease and is a good evaluation of those categorized as normal or overweight. A waist circumference 40 in for men and 35 in for women is associated with an increased risk of diabetes, dyslipidemia and cardiovascular disease secondary to excess abdominal fat.
Adipose tissue is a metabolically active endocrine and paracrine organ, and hence more than just a repository for fat. Experimentation on this tissue would undoubtedly increase our understanding of the pre-eclampsia phenotype. Abdominal fat biopsied from women with normal pregnancy exhibits an increase in basal and hormone-stimulated rates of lipolysis in vitro compared to abdominal fat from non-pregnant women (Williams and Coltart, 1978). To date, however, there has been little study of adipose tissue of women with normal, pre-eclamptic, or fetal growth-restricted pregnancy. The role of novel lipid-regulatory factors such as peroxisome proliferator-activated receptors, resistin, and adiponectin in pregnancy adaptation and pathogenesis also await evaluation. Fascinating interactions between adipogenesis and angiogenesis have been noted (Fukumura et al., 2003). Circulating endothelial progenitor cells likely contribute to ongoing endothelial maintenance and repair in the adult...
The initial characterization of SSAT-overexpressing mice revealed, in addition to hairlessness, practically a total lack of subcutaneous fat depots (7). Subsequently, we found that these animals also lacked visceral fat depots and thus were severely lipo-atrophic. In contrast to other lipoatrophic mouse models, SSAT transgenics did not show any triglyceride accumulation in nonadipose tissues and they fully retained insulin sensitivity (21). On fasting, the transgenic animals showed severely impaired ketogenesis, very low plasma leptin level, and significantly reduced triglyceride, glucose, and insulin levels. The transgenic animals also exhibited significantly elevated basal metabolic rate in comparison with the wild-type animals, indicating a greater expenditure of energy (21). It thus appears that generalized SSAT overexpression causes lipoatrophy, but also
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