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

In utero overexposure to glucocorticoids may explain the association between low birth weight and subsequent development of the metabolic syndrome. We previously showed that prenatal dexamethasone (dex) exposure in the rat lowers birth weight and programs adult fasting and postprandial hyperglycemia, associated with increased hepatic gluconeogenesis driven by elevated liver glucocorticoid receptor (GR) expression. This study aimed to determine whether prenatal dex (100 microg/kg per day from embryonic d 15 to embryonic d 21) programs adult GR expression in skeletal muscle and/or adipose tissue and whether this contributes to altered peripheral glucose uptake or metabolism. In utero dex-exposed rats remained lighter until 6 months of age, despite some early catch-up growth. Adults had smaller epididymal fat pads, with a relative increase in muscle size. Although glycogen storage was reduced in quadriceps, 2-deoxyglucose uptake into extensor digitorum longus muscle was increased by 32% (P < 0.05), whereas uptake in other muscles and adipose beds was unaffected by prenatal dex. GR mRNA was not different in most muscles but selectively reduced in soleus (by 23%, P < 0.05). However, GR mRNA was markedly increased specifically in retroperitoneal fat (by 50%, P < 0.02). This was accompanied by a shift from peroxisomal proliferator-activated receptor gamma 1 to gamma 2 expression and a reduction in lipoprotein lipase mRNA (by 28%, P < 0.02). Adipose leptin, uncoupling protein-3 and resistin mRNAs, muscle GLUT-4, and circulating lipids were not affected by prenatal dex. These data suggest that hyperglycemia in 6-month-old rats exposed to dexamethasone in utero is not due to attenuated peripheral glucose disposal. However, increased GR and attenuated fatty acid uptake specifically in visceral adipose are consistent with insulin resistance in this crucial metabolic depot and could indirectly contribute to increased hepatic glucose output.
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PMID:Programming of rat muscle and fat metabolism by in utero overexposure to glucocorticoids. 1258 77

Microalbuminuria clusters with the metabolic syndrome, and both conditions predict cardiovascular disease mortality. The reported relationships of microalbuminuria with the individual components of the metabolic syndrome (i.e., hyperglycemia, insulin resistance, hypertension, dyslipidemia, abdominal obesity) are variable. Each of these components, as well as intrauterine effects and diet and other lifestyle factors, may contribute to elevated risk of microalbuminuria in certain population groups. Recent evidence indicates a role for oxidation and inflammation in cardiovascular disease, and endothelial dysfunction (exacerbated by factors such as dyslipidemia) may be the mediator of this relationship. Because endothelial dysfunction can also be manifested as microalbuminuria, this provides a potential explanation of the observed association of the metabolic syndrome, chronic inflammation, and microalbuminuria.
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PMID:Association of albuminuria and the metabolic syndrome. 1264 50

The metabolic syndrome often develops into and is usually present in type 2 diabetes in association with premature cardiovascular disease. Treating diabetes can prevent some of its devastating consequences, but it does not eliminate them all. With the goal to eliminate all the adverse consequences of the syndrome, the optimal approach would be through its prevention. Insulin resistance appears to be pivotal to development of the syndrome complex that includes features such as intra-abdominal or visceral obesity, hypertension, impaired glucose homeostasis, dyslipidemia with elevated triglycerides and low high-density lipoprotein without elevations of low-density lipoprotein, a procoagulant state, and impaired vascular function. Improving the insulin resistance needs to be the primary target of the therapy. Hyperglycemia, which is one feature of the metabolic syndrome, may range from impaired glucose tolerance (IGT) to overt diabetes. The risk of progression of the disease from IGT to diabetes is increased with time and the presence of various risk factors. Diabetes is a disease of serious concern because of the associated complication of the disease and the huge impact on the health care costs. Many short- and longer-term trials have shown promise in the prevention of diabetes and its metabolic and cardiovascular consequences.
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PMID:Preventing diabetes by treating aspects of the metabolic syndrome. 1264 67

Hyperinsulinemia and other associated metabolic factors, including hyperglycemia, dyslipidemia, hypertension, and central obesity lead to increased cardiovascular risk and indicate a metabolic syndrome. Levels of fasting insulin were measured in an ethnic Gipsy minority group (n=149) and compared to the majority Slovak population (n=197). The average insulin level was significantly increased in the minority group with a 21% risk value vs 5%. Hyperglycemia was equal in both groups (17% in Gipsy group, 16% in majority group). The incidence of other risk factors for cardiovascular disease and metabolic syndrome is greater in the Gipsy group (47% vs 38%--hypertriacylglycerolemia, 62% vs 46%--HDL-cholesterol level below safety limit, 16% vs 10%--systolic hypertension, 20% vs 11%--diastolic hypertension, 36% vs 22%--obesity). The results of hyperinsulinemia, hypertriacylglycerolemia, hypo-HDL-cholesterolemia, hypertension and obesity indicate, that the Gipsy population is at higher risk for cardiovascular disease. (Tab. 1, Fig. 1, Ref. 12.).
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PMID:Insulin levels in Gipsy minority. 1269 73

Over the last decade, new factors including endothelial dysfunction, vascular inflammation, and abnormalities of blood coagulation have joined more established components of the metabolic syndrome, such as hyperglycemia, hypertension, dyslipidemia, and visceral obesity. Many of these factors are known to promote atherosclerosis and the clustering of metabolic abnormalities within the syndrome makes a major contribution to the increased risk of cardiovascular disease and death associated with type 2 diabetes. Given that most patients have multiple cardiovascular risk factors, good glycemic control does not, by itself, adequately reduce the burden of cardiovascular disease associated with diabetes and clinical management needs to address the full profile of cardiovascular risk. The thiazolidinediones have potentially beneficial effects on many components of the metabolic syndrome and so may help to improve cardiovascular outcomes in type 2 diabetes.
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PMID:The expanding scope of the metabolic syndrome and implications for the management of cardiovascular risk in type 2 diabetes with particular focus on the emerging role of the thiazolidinediones. 1281 Feb 46

The metabolic syndrome is a highly prevalent clinical entity. The recent Adult Treatment Panel (ATP III) guidelines have called specific attention to the importance of targeting the cardiovascular risk factors of the metabolic syndrome as a method of risk reduction therapy. The main factors characteristic of this syndrome are abdominal obesity, atherogenic dyslipidemia, elevated blood pressure, insulin resistance (with or without glucose intolerance), prothrombotic and proinflammatory states. An insulin resistance following nuclear peroxisome proliferator activated receptors (PPAR) deactivation (mainly obesity-related) is the key phase of metabolic syndrome initiation. Afterwards, there are 2 principal pathways of metabolic syndrome development: 1) with preserved pancreatic beta cells function and insulin hypersecretion which can compensate for insulin resistance. This pathway leads mainly to the macrovascular complications of metabolic syndrome; 2) with massive damage of pancreatic beta cells leading to progressively decrease of insulin secretion and to hyperglycemia (e.g. overt type 2 diabetes). This pathway leads to both microvascular and macrovascular complications. We suggest that a PPAR-based appraisal of metabolic syndrome and type 2 diabetes may improve our understanding of these diseases and set a basis for a comprehensive approach in their treatment.
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PMID:Metabolic syndrome and type 2 diabetes mellitus: focus on peroxisome proliferator activated receptors (PPAR). 1283 41

Cardiovascular disease is a leading cause of death and disability in patients with diabetes or metabolic syndrome (MS). The available data suggest that many patients with diabetes or MS already have vascular abnormalities by the time they are diagnosed with their metabolic disorder. Endothelial dysfunction (ED), which is one of the initial steps in the process of vascular disease, is often present in patients with diabetes or MS. Although the precise mechanism(s) by which diabetes or MS causes ED remains to be elucidated, several possibilities exist. Hyperglycemia, hyperinsulinemia, increased oxidative stress, and diabetic dyslipidemia can all contribute to ED individually or in concert with one another. ED in the setting of diabetes or MS can subsequently result in the activation of a variety of pathways that alter vascular function and participate in the process of vascular remodeling and atherosclerosis. Because insulin resistance is the predominant mechanism responsible for various perturbations seen in MS or diabetes, it is essential to develop a therapeutic strategy that can improve insulin sensitivity with the hope that such interventions would reduce the risk of future cardiovascular events.
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PMID:Mechanisms of endothelial dysfunction in the metabolic syndrome. 1286 90

The recent focus on emerging cardiovascular risk factors, such as C-reactive protein, homocysteine, and small, dense low-density lipoprotein (LDL), may give the false impression that the current approach to the assessment of cardiovascular disease risk fails to identify a large section of the high-risk population. On the contrary, the new guidelines of the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) propose classifying an enormous number of individuals, including people with any form of atherosclerotic disease, diabetes, and a combination of major risk factors, into the category of high risk (>20% likelihood of a major coronary event or stroke in 10 years). Considering the widespread prevalence of the metabolic syndrome-a high-risk condition characterized by mild hypertension, mild dyslipidemia, hyperglycemia, and visceral obesity-we may be faced with the challenge of implementing aggressive risk reduction therapies in as much as 30% of the adult US population. From the point of view of risk assessment, a practical approach is to follow the NCEP guidelines (ie, place patients with diabetes and those with atherosclerotic complications in the highest risk category), apply the Framingham calculation to determine risk in people with common risk factors, and initiate early intervention in people who have familial hypercholesterolemia (LDL cholesterol >200 mg/dL) or a family history of early cardiovascular disease. The emerging risk factors may be useful for further stratifying risk in individuals with intermediate risk and the presence of risk factors not included in the Framingham calculation.
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PMID:A practical approach to risk assessment to prevent coronary artery disease and its complications. 1286 51

Several epidemiological studies have shown an association between postprandial hyperglycemia and mortality from cardiovascular disease. Postprandial hyperglycemia is frequently associated with visceral obesity which plays a key role in metabolic abnormalities such as dyslipidemia and hypertension. Inhibitors of alpha-glucosidase and nateglinide have beneficial effects on the metabolic syndrome associated with visceral obesity. Voglibose in combination with diet therapy reduces visceral fat deposition and ameliorates insulin resistance. Acarbose slightly reduces blood pressure of hypertensive diabetic patients. Nateglinide, a rapidly acting insulin secretagogue, lowers postprandial glucose levels without significant body weight gain. These drugs may protect pancreatic beta-cells from postprandial glucose toxicity and prevent the progression of diabetes.
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PMID:[Pharmacological treatment of postprandial hyperglycemia in hypertensive patients with type 2 diabetes mellitus]. 1287 88

In Europid populations, low birth weight of offspring predicts insulin resistance in the mother and cardiovascular disease in both parents. We investigated the association between birth weight of offspring and obesity and cardiovascular risk in the parents of 477 8-year-old children born at the King Edward Memorial Hospital, Pune, India. Eight years after the birth of the child, mothers (33 years of age, n = 459) of heavier babies were taller and more obese (BMI, fat mass, and waist circumference, all P < 0.001) than mothers of lighter babies. Increasing offspring birth weight predicted higher homeostasis model assessment for insulin resistance (P < 0.01) and metabolic syndrome in mothers (P < 0.001) (adjusted for offspring sex and birth order, maternal age, and socioeconomic status) but not hyperglycemia. Fathers (39 years of age, n = 398) of heavier babies were taller and heavier, independent of maternal size (P < 0.01, both), but were not more insulin resistant. Unlike other reports, lower offspring birth weight did not predict insulin resistance in fathers. Thus, urban Indian parents have a higher risk of being obese 8 years after delivery of a heavier child. Mothers but not fathers of heavier babies also have a higher risk of being insulin resistant and developing the metabolic syndrome. Our findings highlight the need for a better understanding of the relation between fetal growth and future health before contemplating public health interventions to improve fetal growth.
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PMID:Higher offspring birth weight predicts the metabolic syndrome in mothers but not fathers 8 years after delivery: the Pune Children's Study. 1288 27


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