Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0311277 (abdominal obesity)
 2,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The insulin resistance syndrome is composed of risk factors for cardiovascular disease, including insulin resistance with hyperinsulinemia, atherogenic dyslipidemia, hypertension, abdominal obesity, and impaired hemostasis. Patients with type 2 diabetes frequently manifest multiple risk factors for cardiovascular morbidity and mortality. Management of the insulin resistance syndrome often includes antihypertensive, lipid-lowering, and antihyperglycemic agents. Because thiazolidinediones (TZDs) directly improve insulin resistance, early use may provide substantial benefits to patients with type 2 diabetes. TZDs reduce plasma glucose and insulin concentrations, promote relocation of body fat, and have anti-inflammatory effects on the vascular endothelium. Combination oral hypoglycemic therapy may be ideal for maintaining adequate glycemic control in patients with type 2 diabetes. The combination of a TZD and a biguanide, which improves insulin sensitivity and lowers blood glucose through different pathways, offers significant benefits and may help prevent or delay prevent complications associated with type 2 diabetes.
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PMID:Insulin resistance syndrome. Description, pathogenesis, and management. 1278 29

Disturbances of lipids metabolism described in obese persons are important factor damaging vascular endothelium. Known markers of endothelium impairment are: von Willebrand factor (vWf), tissue plasminogen activator (t-PA:Ag) and thrombomodulin (TM). The aim of the work was to evaluate markers of the endothelial disturbance in the blood plasma of persons with obesity. The study was performed in the group of 50 obese persons (39 W, 11 M) aged 35-65 (means 48.8) years with abdominal obesity. The control group consisted of 30 healthy volunteers aged 25-56 (means 41.0) years. In the poor platelet plasma obtained from venous citric blood concentrations of TM, von Willebrand factor antigen (vWf:Ag) and tissue plasminogen activator antigen (t-PA:Ag) were determined using immunoenzyme-linked assay (ELISA). In the obese persons significantly higher concentration of vWf:Ag and t-PA:Ag in comparison to control group. Analysis of results obtained according sex showed that in the blood plasma of obese women TM concentration was significantly higher than in healthy women. Our study proved that in the blood plasma of obese men there are evidences of impairment of endothelial function as higher concentration of vWf:Ag and t-PA:Ag, but in the group of obese women as the increased TM concentration.
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PMID:[Thrombomodulin, von Willebrand factor and tissue plasminogen activator in the blood plasma of obese women and men]. 1505 51

Adiponectin is the most abundant peptide secreted by adipocytes, being a key component in the interrelationship between adiposity, insulin resistance and inflammation. Central obesity accompanied by insulin resistance is a key factor in the development of metabolic syndrome (MS) and future macrovascular complications. Moreover, the remarkable correlation between coronary artery disease (CAD) and alterations in glucose metabolism has raised the likelihood that atherosclerosis and type 2 diabetes mellitus (T2DM) may share a common biological background. We summarize here the current knowledge about the influence of adiponectin on insulin sensitivity and endothelial function, discussing its forthcoming prospects and potential role as a therapeutic target for MS, T2DM, and cardiovascular disease. Adiponectin is present in the circulation as a dimer, trimer or protein complex of high molecular weight hexamers, >400 kDa. AdipoR1 and AdipoR2 are its major receptors in vivo mediating the metabolic actions. Adiponectin stimulates phosphorylation and AMP (adenosin mono phosphate) kinase activation, exerting direct effects on vascular endothelium, diminishing the inflammatory response to mechanical injury and enhancing endothelium protection in cases of apolipoprotein E deficiency. Hypoadiponectinemia is consistently associated with obesity, MS, atherosclerosis, CAD, T2DM. Lifestyle correction helps to favorably modify plasma adiponectin levels. Low adiponectinemia in obese patients is raised via continued weight loss programs in both diabetic and nondiabetic individuals and is also accompanied by reductions in pro-inflammatory factors. Diet modifications, like intake of fish, omega-3 supplementation, adherence to a Mediterranean dietary pattern and coffee consumption also increase adiponectin levels. Antidiabetic and cardiovascular pharmacological agents, like glitazones, glimepiride, angiotensin converting enzyme inhibitors and angiotensin receptor blockers are also able to improve adiponectin concentration. Fibric acid derivatives, like bezafibrate and fenofibrate, have been reported to enhance adiponectin levels as well. T-cadherin, a membrane-associated adiponectin-binding protein lacking intracellular domain seems to be a main mediator of the antiatherogenic adiponectin actions. The finding of novel pharmacologic agents proficient to improve adiponectin plasma levels should be target of exhaustive research. Interesting future approaches could be the development of adiponectin-targeted drugs chemically designed to induce the activaton of its receptors and/or postreceptor signaling pathways, or the development of specific adiponectin agonists.
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PMID:Adiponectin: a manifold therapeutic target for metabolic syndrome, diabetes, and coronary disease? 2495 99