Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0497406 (overweight)
 26,365 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prevalence of mild and moderate hypercholesterolemia among the middle-aged population of the G.D.R. is about 30%. Thus, this is the most important risk factor for coronary heart diseases. Primary therapeutic techniques are elimination of overweight, low-fat diet, rich in monoenic and polyenic acids, and increase of physical activity. When by these measures a decrease of cholesterol to 5.2-5.5 mmol/l is not achieved the introduction of lipid drugs is to be considered in dependence on the individual risk (associated risk factors like smoking, hypertension, diabetes, low HDL-cholesterol). In case of mild to moderate polygenic hypercholesterolemia cholestyramine, nicotinic acid and modern fibrates have the priority. Familial hypercholesterolemia demands as a rule the introduction of statins (e.g. lovastatin) or combinations of the above mentioned lipid drugs or the combination of cholestyramine and lovastatin, resp. In this way the prognosis even of patients with severe familial hypercholesterolemia can be improved decisively. Considering the fact that this would be a life-accompanying therapy a thorough consideration of the risk/benefit ratio and an adequate medical supervision are necessary.
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PMID:[Guidelines for the treatment of hypercholesterolemia]. 224 95

In conclusion, many drugs have been used as lipid lowering agents. Only five currently combine efficacy and acceptable side effects. None of these, nicotinic acid, clofibrate, probucol, cholestyramine or colestipol, is without serious drawbacks. In using lipid lowering drugs, it is important to bear in mind the following. First, no patient should be committed to an indefinite period of drug therapy without an adequate trial of diet therapy. For overweight patients, caloric restriction and weight reduction should always be therapeutic goals. Second, as our understanding of lipoprotein metabolism increases, evaluation of new drugs must include not only their effects on triglyceride but also on lipoprotein and apoprotein levels. Third, our drug armamentarium is currently quite limited and there is a pressing need for the development of new, safe and effective hypolipidemic agents.
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PMID:The mechanism of action of lipid-lowering drugs. 712 96

Because patients with low high-density lipoprotein (HDL) cholesterol (HDL-C) are at high risk for clinical coronary artery disease (CAD) events, these patients require aggressive treatment with lifestyle modifications-increased exercise, smoking cessation, and weight loss in overweight patients-and available pharmacological agents. Drugs that raise HDL-C include nicotinic acid, fibric acid derivatives, estrogens, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins), alpha-blockers, and alcohol. However, all agents that increase HDL-C may not have the same clinical benefit, just as, as shown in genetic studies in humans and mice, genetic causes of high HDL-C do not always protect against CAD, nor do genetic causes of low HDL-C always increase risk for CAD. Better understanding of the complexities of HDL metabolism and the mechanisms by which HDL protects against CAD is needed to enable the development of new therapeutic strategies--novel drugs or gene delivery systems--to increase HDL-C and reduce CAD events. The statins are the agents with the greatest evidence for slowing progression of CAD and reducing clinical events in patients with low HDL-C, but additional research is needed to determine the potential benefits of additional interventions that increase HDL-C, including combination therapy, which may provide greater improvements in the entire lipid profile.
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PMID:Defining specific goals of therapy in treating dyslipidemia in the patient with low high-density lipoprotein cholesterol. 979 Apr 15

Scientific evidence continues to accumulate regarding fasting serum triglycerides as an independent risk factor for coronary heart disease. In response, the National Cholesterol Education Program has revised the acceptable level of fasting triglycerides from <200 mg/dL to <150 mg/dL. A significant percentage of Americans suffer from hypertriglyceridemia, and considering the expanding numbers of individuals who are physically inactive, overweight, and suffering from the metabolic syndrome, it is expected that these numbers will continue to rise over the next decade. Fortunately, nutraceutical and lifestyle options have been shown to substantially and consistently reduce this risk factor. This review will focus on management options for the hypertriglyceridemic patient with an emphasis on nicotinic acid, pantethine, fish oils (eicosapentaenoic and docosahexaenoic acids), and modified carbohydrate diets.
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PMID:Dietary and nutraceutical options for managing the hypertriglyceridemic patient. 1676 Jun 91

RELATIONSHIP BETWEEN HDL-C AND CARDIOVASCULAR DISEASES: Beyond the role of low-density lipoprotein cholesterol (LDL-c) in the development of atherosclerosis, growing evidence suggest that high-density lipoprotein cholesterol (HDL-c) is a powerful predictor of cardiovascular disease. Indeed, epidemiological, mechanistic and intervention studies suggest that low HDL-c is a major cardiovascular risk factor and that increasing HDL-c plasma levels may be beneficial, particularly in patients with low HDL-c levels. The inverse association between HDL-c concentrations and cardiovascular risk is continuous without threshold value. Thus, any categorical definition of low HDL-c is arbitrary. PROTECTIVE EFFECTS OF HDL: HDL particles are highly heterogeneous in structure and intravascular metabolism. Antiatherogenic properties of HDL include its role in the reverse cholesterol transfer, besides its antioxidant, anti-inflammatory and antiapoptotic activities. WHAT SHOULD CLINICIANS DO?: From a practical point of view, HDL-c should be systematically measured to assess the cardiovascular risk in patients. The first step to consider in subjects with low HDL-c is to look for specific causes and give advice to change inappropriate lifestyle components associated with low HDL-c, such as smoking, lack of physical exercise and overweight. Patients with very low HDL-c need a thorough evaluation by specialist physicians. Statins are associated with a modest increase of HDL-c (5%) while fibrates and nicotinic acid increase HDL-c by 10% and 20% respectively.
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PMID:HDL-c is a powerful lipid predictor of cardiovascular diseases. 1793 41

Worldwide breast cancer (BC) constitutes a significant public health concern. Excess body weight is associated with postmenopausal BC (PBC) risk. Recent studies have shown that the constellation of obesity, insulin resistance and serum adipokine levels are associated with the risk and prognosis of PBC. Nicotinamide phosphoribosyl-transferase (Nampt), also known as visfatin and pre-B-cell-colony-enhancing factor, found in the visceral fat, represents a novel pleiotropic adipokine acting as a cytokine, a growth factor and an enzyme. It plays an important role in a variety of metabolic and stress responses as well as in the cellular energy metabolism, particularly NAD biosynthesis. Nampt exhibits proliferative, anti-apoptotic, pro-inflammatory and pro-angiogenic properties. Nampt's insulin-mimetic function remains a controversial issue. Circulating Nampt levels are increased in obese women. Also, Nampt levels are significantly elevated in women suffering from PBC than in healthy controls independently from known risk factors of BC, anthropometric and metabolic parameters as well as serum concentrations of well known adipokines. High expression of Nampt in BC tissues was reported to be associated with more malignant cancer behavior as well as adverse prognosis. Taking into account the mitogenicity of Nampt as well as its proliferative, anti-apoptotic and pro-angiogenic properties, a novel hypothesis is proposed whereas Nampt may be involved in the etiopathogenesis of PBC and may represent a missing link between overweight/obesity and PBC. Nampt could exert its effects on the normal and neoplastic mammary tissue by endocrine and paracrine mechanisms; Nampt could also be secreted by tumor epithelial cells in an autocrine manner. It could stimulate mammary epithelial cell proliferation, invasion, metastasis, and angiogenesis, which is essential for BC development and progression. Serum Nampt might be a novel risk factor as well as a potential diagnostic and prognostic biomarker in PBC. In addition, pharmacologic agents that neutralize biochemically Nampt or medications that decrease Nampt levels or downregulate signaling pathways downstream of Nampt may prove to be useful anti-cancer agents. The potential harmful effect on PBC risk due to vitamin B3 (nicotinic acid, a natural NAD precursor in the biosynthetic route leading to NAD) intake is speculated for the first time. In this hypothesis, the role of Nampt in BC carcinogenesis and progression is explored as well as the pathophysiological mechanisms that underlie the association between Nampt and PBC in the context of a dysfunctional adipose tissue in obesity. Understanding of these mechanisms may be important for the development of preventive and therapeutic strategies against PBC.
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PMID:Nicotinamide phosphoribosyl-transferase/visfatin: a missing link between overweight/obesity and postmenopausal breast cancer? Potential preventive and therapeutic perspectives and challenges. 2292 56