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

The term "reverse epidemiology" is used to indicate that such surrogates of cardiovascular risk and metabolic syndrome as obesity, hypercholesterolemia and hypertension are paradoxically associated with greater survival in individuals with chronic disease states and wasting, including dialysis patients, in whom the short-term survival is the issue at hand. It is being debated whether the crossing curves of the obesity-mortality association in dialysis patients vs. the general population reflect the residual confounding that needs to be controlled away statistically, or whether they have biological plausibility in sharp contradistinction to the currently dominating Framingham paradigm. In the rush to define the crossing curves as statistical artifact and to dismiss the term "reverse epidemiology" as a misnomer, we may miss the opportunity to gain information housed in those crossing lines and may miss the bigger picture, i.e., how to improve longevity in dialysis patients. Even though some of the survival paradoxes in dialysis patients appear to fulfill the Hill's criteria of causation, there are still two major drawbacks: (1) convincing pathophysiologic pathways to link dialysis patient survival to obesity, fat accumulation, higher serum lipoprotein levels or slightly higher than normal blood pressure values are yet to be verified in animal and other scientifically sound models; and (2) randomized controlled trials need to show that nutritional interventions resulting in weight gain can lead to greater survival in dialysis patients. Studying the survival paradoxes may lead to a paradigm shift by establishing targets beyond the Framingham guidelines for populations with chronic disease states.
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PMID:What is so bad about reverse epidemiology anyway? 1799 Dec 10

Obesity is a complex, multifactorial chronic disease frequently associated with cardiovascular risks, hypertriglyceridemia, low high-density lipoprotein-cholesterol, high blood pressure, and the insulin resistance that appears to be central to the pathogenesis of Type II diabetes. Plasminogen activator inhibitor-1 expression induced in differentiating adipose tissue, but its role in adipogenesis and obesity is poorly understood. Circulating plasminogen activator inhibitor-1 levels are elevated at an early stage of impaired glucose tolerance, resulting in diabetes and metabolic syndrome. Plasminogen activator inhibitor-1 levels are also significantly elevated in the plasma of obese individuals and in adipose tissues of obese mice and humans. Some investigators proposed that the -675 4G/5G polymorphism in plasminogen activator inhibitor-1 promoter caused overexpression of this gene and predisposed carriers to obesity. In this study, we investigated the role of -675 4G/5G polymorphism in plasminogen activator inhibitor-1 promoter in the expression of this gene and the contribution of plasminogen activator inhibitor-1 to adipogenesis. Using a dual-luciferase promoter assay, we determined that the -675 4G/5G polymorphism contributes significantly to overexpression of plasminogen activator inhibitor-1 in the course of adipogenesis. The antidiabetic agents troglitazone and ciglitazone inhibited reporter gene expression driven by wild-type and -675 4G/5G mutant promoter, as well as the expression of endogenous plasminogen activator inhibitor-1, indicating that suppression of plasminogen activator inhibitor-1 expression may contribute to antidiabetic effects of these agents. The results indicate that absence of plasminogen activator inhibitor-1 in adipocytes may protect the cells against insulin resistance by promoting glucose uptake and adipocyte differentiation via a decrease in the peroxisome proliferator activated receptor-gamma expression that modulates the adipocyte differentiation.
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PMID:The effect of plasminogen activator inhibitor-1 -675 4G/5G polymorphism on PAI-1 gene expression and adipocyte differentiation. 1816 May 87

Epidemiological and animal studies show that small changes in the developmental environment can induce phenotypic changes affecting an individual's responses to their later environment. These may alter the risk of chronic disease such as metabolic syndrome or cardiovascular disease. Recent research shows that animals exposed to such a mismatch between prenatal and postnatal environment develop obesity, reduced activity, leptin and insulin resistance, elevated blood pressure and vascular endothelial dysfunction. Epigenetic processes are involved in such effects, targeted to promoter regions of specific genes in specific tissues. Such fine control of gene expression suggests that the mechanisms have been retained through evolution through their adaptive advantage, rather than representing extreme effects of developmental disruption akin to teratogenesis. There may be adaptive advantage in a developmental cue inducing a phenotypic change in generations beyond the immediate pregnancy, and a range of data that support this concept. In animals, epigenetic effects such as DNA methylation can be passed to successive generations. Environmental toxins, including endocrine disruptors, may induce greater risk of chronic disease, even at low exposure levels, if they affect such normal developmental epigenetic processes. Appropriate interventions may have long-term multigenerational effects to reduce the risk of chronic disease.
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PMID:Developmental origins of health and disease: new insights. 1822 60

The prevalence and etiology of nongenetic causes of obesity are reviewed, along with obesity-associated comorbidities of the metabolic syndrome. The role of nongenetic causes of obesity from environmental affluences, central nervous system developmental effects in adult obesity, and psychosocial disorders affecting obesity through central nervous system dysfunction are discussed. Obesity is now the major underlying cause of the metabolic syndrome and its alarmingly increased prevalence worldwide makes it the most preventable cause of chronic disease burden.
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PMID:The prevalence and etiology of nongenetic obesity and associated disorders. 1836 Mar 36

Lifestyle and diet play important roles in the development of cardiovascular disease (CVD), which is the leading cause of death in Western countries. Metabolic syndrome, which is characterized by a group of metabolic risk factors, is associated with the subsequent development of type 2 diabetes and CVD. Epidemiological studies have documented that nutritional factors may affect the prevalence of the metabolic syndrome. Beyond weight control and reduction of total calories, the diet should be low in saturated fats, trans fats, cholesterol, sodium, and simple sugars. In addition, there should be ample intake of fruits, vegetables, whole grains, and monounsaturated fat; fish intake should be encouraged. These features are very reminiscent of the nutritional principles currently used to define the Mediterranean-style diet. This diet's high fiber content, n-3 fatty acids, and antioxidants, as well as phytochemicals from olive oil, legumes, whole grains, fruits, and vegetables, might be responsible for its beneficial effect on the health of metabolic syndrome patients. This may occur through the reduction of systemic vascular inflammation and endothelium dysfunction without having a drastic effect on body weight. The choice of healthy sources of carbohydrates, fat, and proteins, associated with regular physical activity and avoidance of smoking, is critical to fighting the war against chronic disease.
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PMID:Diet and the metabolic syndrome. 1837 Jul 98

Magnesium plays a role in a number of chronic, disease-related conditions. This article reviews current pertinent literature on magnesium, focusing on hypertension and cardiovascular diseases and implications for relationships with diabetes and metabolic syndrome. A major role for magnesium is in the regulation of blood pressure. While data are not entirely consistent, it does appear that an inverse relationship between magnesium intake and blood pressure is strongest for magnesium obtained from food rather than that obtained via supplements. Hypertension associated with preeclampsia appears to be alleviated when magnesium is administered; in addition, women with adequate intakes of magnesium are less likely to be affected by preeclampsia than those with an inadequate intake. A role for magnesium in other cardiovascular diseases has been noted in that increased magnesium intake may improve serum lipid profiles. Dietary magnesium is also recommended to aid in the prevention of stroke and is important for skeletal growth and development. Magnesium may also play a role in the development of diabetes mellitus, obesity, and metabolic syndrome. There are data from some studies, such as the DASH and PREMIER studies, that suggest that lifestyle changes (including adequate magnesium intake) can benefit blood pressure control, promote weight loss, and improve chronic disease risk.
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PMID:Magnesium in hypertension, cardiovascular disease, metabolic syndrome, and other conditions: a review. 1839 Jul 81

Paediatric Human Immunodeficiency Virus infection (HIV) nowadays is a chronic disease with an excellent long term prognosis, but lifelong combined antiretroviral treatment is required. However, an improved quality of life in this population is limited by adverse drug effects. The highest risk of treatment toxicity is developing a complete metabolic syndrome including: Hyperlipemia, lipodystrophy, insulin resistance, lactic acidosis, osteopenia, hypertension, and specific system and organ toxicity, such as the kidney, liver, CNS or bone marrow. The risk of cardiovascular disease adult life and also definitive bone mass damage are the most significant metabolic costs that have to paid for increased survival. Most of these toxicities were able to be adequately treated but, pharmacological interferences, patient intolerance and the high number of drugs are the problems that limit the adherence to treatment, which is essential for a good therapeutical efficacy. In this article, we present four HIV paediatric patients who presented with almost the whole range of metabolic toxicities, and a practical overview of therapeutical management.
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PMID:[Antiretroviral drug toxicity in human immunodeficiency virus infected children]. 1844 85

There is an intrinsic complexity in the pathogenesis of common diseases. The concept of gene-environment interaction is receiving support from emerging evidence coming primarily from studies involving diet and cardiovascular disease (CVD) and its various risk factors. The accumulating evidence shows that common variants at candidate genes for lipid metabolism, inflammation, and obesity are associated with altered plasma levels of classic and new biomarkers of metabolic syndrome and CVD risk. Major contributors to this knowledge have been a series of large population studies containing phenotype-rich databases and dietary information to which genetic data have been added. Although this approach has provided strong evidence supporting the concept of gene-diet interactions modulating CVD risk factors, the strength of the individual effect is very small, and the replication among studies is rather disappointing. Current population studies are starting to incorporate experimental and analytical approaches that could provide more solid and comprehensive results. However, other limitations, such as the size of the populations required to examine higher-level interactions, are still major obstacles to translating this knowledge into practical public health applications. Nevertheless, data from numerous molecular and genetic epidemiological studies provide tantalizing evidence suggesting that gene-environment interactions, i.e., the modulation by a genetic polymorphism of a dietary component effect on a specific phenotype (e.g., cholesterol levels and obesity), can interact in ways that increase the risk for developing chronic disease, including susceptibility to developing the metabolic syndrome. Once further experience is gained from patients and/or individuals at high risk, more personalized genetic-based approaches may be applied toward the primary prevention and treatment of CVDs and other complex inflammatory diseases.
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PMID:Gene-environment interactions and susceptibility to metabolic syndrome and other chronic diseases. 1867 4

Foetal growth from conception to birth is a complex process predetermined by the genetic configuration of the foetus, the availability of nutrients and oxygen to the foetus, maternal nutrition and various growth factors and hormones of maternal, foetal and placental origin. Maintenance of the optimal foetal environment is the key factor of the future quality of life. Such conditions like inadequate nutrition and oxygen supply, infection, hypertension, gestational diabetes or drug abuse by the mother, expose the foetus to nonphysiological environment. In conditions of severe intrauterine deprivation, there is a potential loss of structural units within the developing organ systems affecting their functionality and efficiency. Extensive human epidemiologic and animal model data indicate that during critical periods of prenatal and postnatal mammalian development, nutrition and other environmental stimuli influence developmental pathways and thereby induce permanent changes in metabolism and chronic disease susceptibility. The studies reviewed in this article show how environmental factors influence a diverse array of molecular mechanisms and consequently alter disease risk including diseases such as metabolic syndrome and cardiovascular diseases, insulin resistance and diabetes mellitus, neuropsychiatric disorders, osteoporosis, asthma and immune system diseases.
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PMID:Nongenomic memory of foetal history in chronic diseases development. 1898 84

We assessed the association of four diet quality scores with multiple cardio-metabolic outcomes among Guatemalan young adults experiencing the nutrition transition. We obtained cross-sectional dietary, demographic, anthropometric and cardio-metabolic risk factor data from 1220 Guatemalan adults (mean age 32.7 (sd 5.8) years) in 2002-4, and computed a Recommended Food Score (RFS), Not Recommended Food Score (NRFS), Food Variety Score (FVS) and the Dietary Quality Index-International (DQI-I). All four scores were correlated with energy intake (r 0.23-0.49; all P < 0.01), but had varying associations with socio-demographic characteristics, lifestyle factors and nutrient intakes. None of the scores was inversely associated with the metabolic syndrome or its components; rather some were positively associated with risk factors. Among both men and women the DQI-I was positively associated with BMI (kg/m2; beta = 0.10, 95 % CI 0.003, 0.21 (men); beta = 0.07, 95 % CI 0.01, 0.14 (women)) and waist circumference (cm; beta = 0.02, 95 % CI 0.01, 0.03 (men); beta = 0.02, 95 % CI = 0.01, 0.02 (women)). Among men, the RFS was positively associated with TAG (mg/l; beta = 0.11, 95 % CI 0.02, 0.21) and glucose (mg/l; beta = 0.13: 95 % CI 0.03, 0.22). We conclude that indices of diet quality are not consistently associated with chronic disease risk factor prevalence in this population of Guatemalan young adults.
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PMID:Diet scores and cardio-metabolic risk factors among Guatemalan young adults. 1902 21


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