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)

In animals deprived of food for a long period, a drop in the fat mass below 5% of the total body mass results in an increase in blood glucocorticoids and uric acid levels, followed by foraging activity. Since the glucocorticoids increase the uric acid excretion, an increase in the level of uric acid in the bladder urine could be the signal for this feeding behaviour and subsequent fat storage. Accumulation of fat is associated with hyperglycaemia, hyperinsulinaemia, hyperlipidaemia, and hypercholesterolaemia as seen in the metabolic syndrome or hibernation. It is hypothesized that uric acid or its structurally related compound, 1-methyl uric acid (one of the metabolites of the methyl xanthines namely caffeine, theophylline, and theobromine present in coffee, tea, cocoa, and some drugs), can act on the urinary bladder mucosa and increases the blood glucose, insulin, triglyceride, and cholesterol levels. In rats, perfusion of the urinary bladder with saturated aqueous solution of uric acid or 1-methyl uric acid results in a significant increase in the serum levels of glucose, insulin, true triglyceride, and total cholesterol in comparison with perfusion of the bladder with distilled water at 20, 40, and 80 min. The uric acid or the 1-methyl uric acid acts on the urinary bladder mucosa and increases the serum glucose, insulin, true triglyceride, and total cholesterol levels.
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PMID:Uric acid or 1-methyl uric acid in the urinary bladder increases serum glucose, insulin, true triglyceride, and total cholesterol levels in Wistar rats. 1524 98

We studied the influence of native lipoproteins on the activity of the angiotensin-converting enzyme (ACE). Lipoproteins of blood serum were inhibiting the activity of soluble ACE. The ACE activity in blood serum was found to depend on a concentration of total cholesterol and of triglycerides. The maximal ACE activity was observed at a concentration of total cholesterol of 9.41 mM/l and at a concentration of triglycerides of 3.05 mM/l. The albumin-linked non-etherified fatty acids affected the ACE activity neither in water solutions nor in presence of lipoprotein complexes. According to the study, the progression of most frequent atherogenic hyperlipidemia results in a 2-fold increase of the ACE activity. It is suggested that an intensified ACE activity in blood plasma can be regarded as an integral component of biochemical disorders in metabolic syndrome.
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PMID:[Lipoproteins of blood serum and the activity of angiotensin-converting enzyme]. 1564 28

This study tested the hypothesis that chronically elevated oxidant stress contributes to impaired active hyperemia in skeletal muscle of obese Zucker rats (OZR) vs. lean Zucker rats (LZR) through progressive deteriorations in microvascular structure. Twelve-week-old LZR and OZR were given 4-hydroxy-2,2,6,6-tetramethylpiperidine 1-oxyl (tempol) in the drinking water for approximately 4 wk. Subsequently, perfusion of in situ gastrocnemius muscle was determined during incremental elevations in metabolic demand, while a contralateral skeletal muscle arteriole and the gastrocnemius muscle was removed to determine dilator reactivity, vessel wall mechanics, and microvessel density. Under control conditions, active hyperemia was impaired at all levels of metabolic demand in OZR, and this was correlated with a reduced microvessel density, increased arteriolar stiffness, and impaired dilator reactivity. Chronic tempol ingestion improved perfusion during moderate to high metabolic demand only and was associated with improved arteriolar reactivity and microvessel density; passive vessel mechanics were unaltered. Combined antioxidant therapy and nitric oxide synthase inhibition in OZR prevented much of the restored perfusion and microvessel density. In LZR, treatment with N(omega)-nitro-L-arginine methyl ester (L-NAME) hydrochloride and hydralazine (to prevent hypertension) impaired active hyperemia, dilator reactivity, and microvessel density, although arteriolar distensibility was not altered. These results suggest that with the development of the metabolic syndrome, chronic reductions in nitric oxide bioavailability, in part via the scavenging actions of oxidative free radicals, contribute to a loss of skeletal muscle microvessels, leading to impaired muscle perfusion with elevated metabolic demand.
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PMID:Reduced nitric oxide bioavailability contributes to skeletal muscle microvessel rarefaction in the metabolic syndrome. 1601 46

Tea is one of the most widely consumed beverages in the world, next only to water. It can be categorized into three types, depending on the level of fermentation, i.e., green (unfermented), oolong (partially fermented) and black (fermented) tea. In general, green tea has been found to be superior to black tea in terms of antioxidant activity owing to the higher content of (-)-epigallocatechin gallate. The processes used in the manufacture of black tea are known to decrease levels of the monometric catechins to a much greater extent than the less severe conditions applied to other teas. The cardioprotective effect of flavonoids from green tea can be attributed to not only antioxidant, antithrombogenic and anti-inflammatory properties but also improvement of coronary flow velocity reserve. In this article, I will discuss the effects of green tea on atherosclerosis, coronary heart disease, hypertension, diabetes, metabolic syndrome and obesity, and, finally, its comparison with black tea.
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PMID:All teas are not created equal: the Chinese green tea and cardiovascular health. 1597 86

Aldosterone is a mineralocorticoid hormone that regulates blood pressure and salt/water balance. Increased aldosterone levels are found in states of disturbed energy balance such as the metabolic syndrome. Adipose tissue has been recognized to play a pivotal role in the regulation of energy homeostasis. We investigated direct aldosterone effects on brown adipocyte function. Aldosterone dose-dependently inhibited expression of uncoupling protein-1 (UCP-1) by 30% (p < 0.01). Furthermore, aldosterone dose-dependently impaired insulin-induced glucose uptake by about 25% (p < 0.01). On a transcriptional level, mRNA of the proinflammatory adipokines leptin and monocyte chemoattractant protein-1 (MCP-1) was increased by 5,000% and 40%, respectively, by aldosterone exposure (p < 0.05). This study demonstrates that aldosterone directly impacts on major adipose functions including stimulation of proinflammatory adipokines.
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PMID:Aldosterone inhibits uncoupling protein-1, induces insulin resistance, and stimulates proinflammatory adipokines in adipocytes. 1603 20

Saturated and trans-fatty acids raise total cholesterol and LDL-cholesterol and are known to increase the risk of CHD, while dietary unsaturated fatty acids play important roles in maintaining cardiovascular health. Replacing saturated fats with unsaturated fats in the diet often involves many complex dietary changes. Modifying the composition of foods high in saturated fat, particularly those foods that are consumed daily, can help individuals to meet the nutritional targets for reducing the risk of CHD. In the 1960s the Dutch medical community approached Unilever about the technical feasibility of producing margarine with a high-PUFA and low-saturated fatty acid composition. Margarine is an emulsion of water in liquid oil that is stabilised by a network of fat crystals. In-depth expertise of fat crystallisation processes allowed Unilever scientists to use a minimum of solid fat (saturated fatty acids) to structure a maximum level of PUFA-rich liquid oil, thus developing the first blood-cholesterol-lowering product, Becel. Over the years the composition of this spread has been modified to reflect new scientific findings and recommendations. The present paper will briefly review the developments in fat technology that have made these improvements possible. Unilever produces spreads that are low in total fat and saturated fat, virtually free of trans-fatty acids and with levels of n-3 and n-6 PUFA that are in line with the latest dietary recommendations for the prevention of CHD. Individuals with the metabolic syndrome have a 2-4-fold increased risk of developing CHD; therefore, these spreads could make a contribution to CHD prevention in this group. In addition, for individuals with the metabolic syndrome the spreads could be further modified to address their unique dyslipidaemia, i.e. elevated blood triacylglycerols and low HDL-cholesterol. Research conducted in the LIPGENE study and other dietary intervention studies will deliver the scientific evidence to justify further modifications in the composition of spreads that are healthy for the heart disease risk factors associated with the metabolic syndrome.
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PMID:Modern fat technology: what is the potential for heart health? 1604 72

The natural history of inborn errors of protein metabolism and the long-term effects of prescribed semisynthetic therapeutic diets are largely unknown. We assessed body composition, measuring body-fat mass and distribution, fat-free mass, total body protein, total body potassium, bone density and skeletal muscle mass, in young adults (age > 18 years; 6 female, 5 male) with inborn errors of protein metabolism maintained on long-term low-protein diets, compared with controls. Female patients were significantly shorter (159.4 cm vs 169.2 cm, p = 0.013) and had higher BMI (25.3 vs 22.0 kg/m2, p < 0.05), abdominal to gluteal circumference ratio (0.84 vs 0.73, p = 0.011), percentage body fat (42.3% vs 29.5%, p < 0.005) and ratio of central to peripheral body fat (1.15 vs 0.86, p < 0.05) than controls. Male patients had lower height-adjusted total body bone mineral content (0.9 vs 1.02 g/m2, p < 0.04) and skeletal muscle mass (31.1 vs 36.3 kg, p < 0.04) than controls. Compared with controls, patients'nitrogen index was significantly lower (0.91 vs 1.03, p < 0.01), consistent with lower total body protein. Potassium index was significantly higher (121.2% vs 110.4%, p < 0.03), consistent with higher body cell mass, or intracellular water. Documentation of body composition in larger patient series is important to elucidate whether these results reflect increased risks (hence opportunities for prevention) of bone disease, metabolic syndrome and cardiovascular disease in this population.
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PMID:Body composition in young adults with inborn errors of protein metabolism--a pilot study. 1615 92

In myocardial damage due to ischemia-reperfusion, the administration of insulin together with glucose and potassium may be protective, although in some patients and animal models, it is ineffective. In a rat model (HTG) with characteristics of the metabolic syndrome, induced by sucrose feeding, ischemia-reperfusion of the isolated heart evidences a less favorable outcome than in control animals, particularly males. We investigated the effect of insulin infusion during the reperfusion period in isolated hearts from control and HTG male and female rats. Weanling Wistar rats were given commercial rat chow and tap water (C rats) or 30% sucrose solution (HTG rats) for 8 months. They developed moderate hypertension and hyperinsulinemia, central adiposity, nephropathy, and hypertriglyceridemia. Cardiac function was recorded in a Langendorff preparation subjected to 25 min ischemia and 15 min reperfusion. The handicapped functionality of HTG hearts is more apparent under conditions of stress. Insulin administration improved particularly mechanical work and +dp/dt max variables. The effect of sex was observed on the type of arrhythmias developed during reperfusion: Only the males showed lethal ventricular fibrillation, which disappeared after insulin administration. Females had lower levels of cardiac enzymes creatine kinase (CKMB) and lactic dehydrogenase (LDH), but their performance was not hindered, probably on account of protective factors such as estrogens. Summing up, the pathological features of the HTG model did not prevent insulin from exerting some of its beneficial effects in HTG hearts. Sex differences in the outcome were more apparent in the type of arrhythmias after reperfusion; they were lethal in HTG males only, but insulin prevented their onset.
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PMID:Isolated heart function during ischemia and reperfusion in sucrose-fed rats: effect of insulin infusion. 1616 99

The early lesions of atherosclerosis begin in childhood, and are related to antecedent cardiovascular disease risk factors. Environmental and genetic factors such as diet, obesity, exercise, and certain inherited dyslipidemias influence the progression of such lesions. The identification of youth at risk for atherosclerosis includes an integrated assessment of these predisposing factors. Treatment starts with a diet low in total and saturated fat and cholesterol, the use of water-soluble fiber and plant sterols, weight control, and exercise. Drug therapy, for example, with inhibitors of hydroxymethylglutaryl CoA reductase, bile acid sequestrants, and cholesterol absorption inhibitors, can be considered in those with a positive family history of premature coronary artery disease and a low-density lipoprotein cholesterol above 160 mg/dL, after dietary and hygienic measures. Candidates for drug therapy often include those with familial hypercholesterolemia, familial combined hyperlipidemia, the metabolic syndrome, polycystic ovarian syndrome, type I diabetes, and the nephrotic syndrome. We review the safety and efficacy of dietary and drug therapy, and propose an updated diagnostic and therapeutic algorithm that includes the metabolic syndrome. The early identification and treatment of youth with dyslipidemias is likely to retard the atherosclerotic process.
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PMID:Treatment of dyslipidemia in children and adolescents. 1625 15

Null mutations of the proopiomelanocortin gene (Pomc) cause obesity in humans and rodents, but the contributions of central versus pituitary POMC deficiency are not fully established. To elucidate these roles, we introduced a POMC transgene (Tg) that selectively restored peripheral melanocortin and corticosterone secretion in Pomc mice. Rather than improving energy balance, the genetic replacement of pituitary POMC in PomcTg mice aggravated their metabolic syndrome with increased caloric intake and feed efficiency, reduced oxygen consumption, increased subcutaneous, visceral, and hepatic fat, and severe insulin resistance. Pair-feeding of PomcTg mice to the daily intake of lean controls normalized their rate of weight gain but did not abolish obesity, indicating that hyperphagia is a major but not sole determinant of the phenotype. Replacement of corticosterone in the drinking water of Pomc mice recapitulated the hyperphagia, excess weight gain and fat accumulation, and hyperleptinemia characteristic of genetically rescued PomcTg mice. These data demonstrate that CNS POMC peptides play a critical role in energy homeostasis that is not substituted by peripheral POMC. Restoration of pituitary POMC expression to create a de facto neuronal POMC deficiency exacerbated the development of obesity, largely via glucocorticoid modulation of appetite, metabolism, and energy partitioning.
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PMID:Glucocorticoids exacerbate obesity and insulin resistance in neuron-specific proopiomelanocortin-deficient mice. 1644 60


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