UMLS:C0948265 - FACTA Search

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Query: UMLS:C0948265 (metabolic syndrome)
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Urotensin II (UII) is an 11 amino acid cyclic peptide originally isolated from the goby fish. The amino acid sequence of UII is exceptionally conserved across most vertebrate taxa, sharing structural similarity to somatostatin. UII binds to a class of G protein-coupled receptor known as GPR14 or the urotensin receptor (UT). UII and its receptor, UT, are widely expressed throughout the cardiovascular, pulmonary, central nervous, renal, and metabolic systems. UII is generally agreed to be the most potent endogenous vasoconstrictor discovered to date. Its physiological mechanisms are similar in some ways to other potent mediators, such as endothelin-1. For example, both compounds elicit a strong vascular smooth muscle-dependent vasoconstriction via Ca(2+) release. UII also exerts a wide range of actions in other systems, such as proliferation of vascular smooth muscle cells, fibroblasts, and cancer cells. It also 1) enhances foam cell formation, chemotaxis of inflammatory cells, and inotropic and hypertrophic effects on heart muscle; 2) inhibits insulin release, modulates glomerular filtration, and release of catecholamines; and 3) may help regulate food intake and the sleep cycle. Elevated plasma levels of UII and increased levels of UII and UT expression have been demonstrated in numerous diseased conditions, including hypertension, atherosclerosis, heart failure, pulmonary hypertension, diabetes, renal failure, and the metabolic syndrome. Indeed, some of these reports suggest that UII is a marker of disease activity. As such, the UT receptor is emerging as a promising target for therapeutic intervention. Here, a concise review is given on the vast physiologic and pathologic roles of UII.
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PMID:Role of urotensin II in health and disease. 2042 34

The objective of this study was to evaluate the effect of metabolic syndrome (MetS) and its individual components on the renal function of patients with type 2 diabetes mellitus (DM). A cross-sectional study was performed in 842 type 2 DM patients. A clinical and laboratory evaluation, including estimated glomerular filtration rate (eGFR) calculated by the modification of diet in renal disease formula, was performed. MetS was defined according to National Cholesterol Education Program - Adult Treatment Panel III criteria. Mean patient age was 57.9 +/- 10.1 years and 313 (37.2%) patients were males. MetS was detected in 662 (78.6%) patients. A progressive reduction in eGFR was observed as the number of individual MetS components increased (one: 98.2 +/- 30.8; two: 92.9 +/- 28.1; three: 84.0 +/- 25.1; four: 83.8 +/- 28.5, and five: 79.0 +/- 23.0; P < 0.001). MetS increased the risk for low eGFR (<60 mL x min(-1) x 1.73 (m2)(-1)) 2.82-fold (95%CI = 1.55-5.12, P < 0.001). Hypertension (OR = 2.2, 95%CI = 1.39-3.49, P = 0.001) and hypertriglyceridemia (OR = 1.62, 95%CI = 1.19-2.20, P = 0.002) were the individual components with the strongest associations with low eGFR. In conclusion, there is an association between MetS and the reduction of eGFR in patients with type 2 DM, with hypertension and hypertriglyceridemia being the most important contributors in this sample. Interventional studies should be conducted to determine if treatment of MetS can prevent renal failure in type 2 DM patients.
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PMID:Effect of metabolic syndrome and of its individual components on renal function of patients with type 2 diabetes mellitus. 2054 38

The results of numerous investigations on the impact of obesity on renal insufficiency conducted in recent years introduce certain dilemmas about their mutual agreement. Some studies suggest that obesity is negatively correlated with the terminal phase of renal failure. On the other hand, other research has shown that reducing the index of body weight of patients with renal disease improves glomerular filtration. Even more confusion comes from findings indicating that metabolic syndrome in non-diabetic renal disease sufferers increases the risk of occurrence and progression of chronic renal disease. However, some research results suggest that obesity is positively correlated with survival of patients on dialysis, i.e., the higher the index of body weight the lower the mortality rate, especially with extremely obese patients. Reverse epidemiology is a term for the medical hypothesis which holds that the influence of obesity and high body weight indexes may be protective and associated with greater survival of obese patients on haemodialysis. A high serum creatinine concentration is a direct consequence of low rates of glomerular filtration and is inversely correlated with mortality rate. However, observations that high creatinine concentrations before haemodialysis treatment are a predictor of survival may be explained by the fact that they are also the direct consequence of increased muscle mass and a higher dietary protein intake. Thus, improvement of their nutritive state might delay progression and diminish the complications expected for patients suffering from kidney insufficiency. The requirements for daily protein intake by dialysis patients are not clear enough, while a hyperprotein diet may be a significant source of uraemic toxins, phosphate and H(+)-ion, which would be detrimental for their health. Some research has indicated that obesity of dialysis patients is not linked to increased risk of cardiovascular diseases in contrast to the general population. On the other hand, a low body mass index and additional parameters of malnutrition are strong independent indicators of mortality rate in dialysis patients. Although, there is a substantial amount of data that support a protective role for obesity, some authors question the existence of the obesity paradox. They do not oppose the results of that research, but suggest that obese individuals are actually protected in the short-term while later on they are liable to higher mortality risks than people of normal body weight. The role of obesity is undisputed as a significant mortality factor in the general population. Nevertheless, some well-designed studies have confirmed that obesity has a protective influence on patients treated by chronic dialysis procedures. This is not to suggest that obesity is recommended as a model for a higher survival rate in those patients, but the role of 'uraemic adipose tissue' and probable additional factors that might result in a lower mortality rate should be considered.
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PMID:Obesity in renal failure--health or disease? 2065 10

Renal cell carcinoma (RCC) affects patients by proliferating in the renal tubules, resulting in renal failure and concomitant urinalysis findings of blood, protein, casts, and abnormal cells in the urine. If untreated, it can spread to the lymph nodes, liver, and lungs. There is currently no proven tumor marker for RCC. The clinical case reported here describes the clinical laboratory findings in a patient with 2 common co-morbidities (metabolic syndrome and alcoholism), who was found to have metastatic renal cell carcinoma at autopsy. Understanding the clinical chemistry of metastatic carcinoma in the presence of common co-morbidities is important for earlier diagnosis and treatment of patients who are most likely to develop these conditions.
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PMID:Metastatic renal cell carcinoma with metabolic syndrome--a case report. 2073 86

In philogenesis, due to the failure to store a great deal of carbohydrates in vivo as glycogen, all animal species began synthesizing from glucose palminitic fatty acid and depositing it as triglycerides. During biological dysfunction of exotrophy (long starvation, early postnatality, hibernation), cells also accomplish a reverse synthesis of glucose from fatty acids under aerobic conditions. Under physiological conditions, acetyl-CoA that is converted to malate and pyruvate in the glyoxalate cycle is a substrate of glyconeogenesis. Under pathological conditions of hypoxia and deficiency of macroerges, gluconeogenesis occurs without ATP consumption through the methylglyoxal pathway when used as a substrate of ketone bodies via the pathway: butyric acid (butyrate) --> beta-hydroxybutyrate --> acetoacetate --> acetone --> acetol --> methylglyoxal --> S-D-lactol-glutathione --> D-lactate --> pyruvate --> D-lactate. Under physiological conditions, this gluconeogenesis pathway does not function. We believe that with low glucose levels in the cell cytosole (glycopenia), under pathological conditions of hypoxia and due to failure to mitochondria to oxidize fatty acids, gene expression and gluconeogenesis occur through the methylglyoxal pathway. At the same time, the cytosol, intercellular environment, and plasma shows the elevated levels of methylglyoxal and D-lactate that it is converted to by the action of glyoxalases I and II. Under pathological conditions, glycopenia develops in starvation, diabetes, and metabolic acidosis, neoplasms, renal failure, and possibly, metabolic syndrome. The chemical interaction of methylglyoxal with the amino acid residues of lysine and arginine results in the denaturation of circulating and structurized proteins via carbonylation--glycosylation.
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PMID:[Methylglyoxal--a test for impaired biological functions of exotrophy and endoecology, low glucose level in the cytosol and gluconeogenesis from fatty acids (a lecture)]. 2073 76

If a lot of carbohydrates cannot be in vivo stored as glycogen, the synthesis of palmitic fatty acid (FA) from glucose and its adipocyte deposition as triglycerides are under way in phylogenesis. With impaired biological function of exotrophy (fasting, early postnatality, hibernation), the cells perform a reverse process--the synthesis of glucose from FA. Physiologically, the substrate of gluconeogenesis is acetyl-CoA that is converted by the malate --> 9 piruvate --> glucose pathway in the glyoxalate cycle. Under the pathological conditions of hypoxia and energy deficiency, gluconeogenesis occurs without ATP consumption via the methylglyoxalate pathway (MGP) while using as a substrate of ketone bodies: butyric acid (butyrate) --> beta-hydroxybutyrate --> acetoacetate --> acetone --> acetol --> methylglyoxal (MG) --> S-D-lactolglutathione --> D-lactate --> piruvate --> D-lactate. Under physiological conditions, this pathway of gluconeogenesis does not work. The authors hold that gene expression and gluconeogenesis occur via the MGP when glucose levels are low in the cell cytosol (glycopenia) and FA cannot be oxidized in the mitochondria. Cytosol, intercellular medium, plasma show elevated levels of MG and D-lactate, to which it converts under the action of glyoxalases I and II. Glycopenia develops in fasting, diabetes mellitus, metabolic syndrome, renal failure, phenofibrate therapy, impaired function of exotrophy--excessive dietary intake of saturated and trans fatty acids. The chemical interaction of MG with amino acid residues of lysine and arginine leads to protein denaturation during carbonylation--glycosylation and impaired biological function of endoecology. The determination of plasma MG and D-lactate may be a test for glycopenia, compensatory activation of gluconeogenesis from FA or for the evaluation of endogenous intoxication.
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PMID:[Methylglyoxal--test for biological dysfunctions of homeostasis and endoecology, low cytosolic glucose level, and gluconeogenesis from fatty acids]. 2134 69

Microalbuminuria has been conclusively established as an independent cardiovascular risk factor, and there is evidence of an association between insulin resistance and microalbuminuria, the former preceding the latter in prospective studies. It has been demonstrated that even the slightest degree of metabolic acidosis produces insulin resistance in healthy humans. Many recent epidemiological studies link metabolic acidosis indicators with insulin resistance and systemic hypertension. The strongly acidogenic diet consumed in developed countries produces a lifetime acidotic state, exacerbated by excess body weight and aging, which may result in insulin resistance, metabolic syndrome, and type 2 diabetes, contributing to cardiovascular risk, along with genetic causes, lack of physical exercise, and other factors. Elevated fruits and vegetables consumption has been associated with lower diabetes incidence. Diseases featuring severe atheromatosis and elevated cardiovascular risk, such as diabetes mellitus and chronic kidney failure, are typically characterized by a chronic state of metabolic acidosis. Diabetic patients consume particularly acidogenic diets, and deficiency of insulin action generates ketone bodies, creating a baseline state of metabolic acidosis worsened by inadequate metabolic control, which creates a vicious circle by inducing insulin resistance. Even very slight levels of chronic kidney insufficiency are associated with increased cardiovascular risk, which may be explained at least in part by deficient acid excretory capacity of the kidney and consequent metabolic acidosis-induced insulin resistance.
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PMID:Metabolic acidosis-induced insulin resistance and cardiovascular risk. 2135 78

Poor early nutrition has varying effects on subsequent cardiometabolic disease (CMD) rates. Fetal and neonatal periods are critical for the development and growth of the systems involved in CMD. The increased rates of hypertension, metabolic syndrome, diabetes mellitus type 2, renal failure and heart failure observed nowadays in Latin America could be the result of the discrepancy between the nutritional environment during fetal and early life and the adult environment. This discrepancy causes a mismatch between the fetal programming of the subject and its adult circumstances created by the imposition of new life styles. The two largest international studies on cardiovascular risk factors for a first myocardial infarction (INTERHEART) and stroke (INTERSTROKE) demonstrated that in Latin America the factor with the highest attributable population risk was abdominal obesity. The conflict between the earlier programming and the later presence of abdominal obesity produced a higher sensitivity of this population to develop a state of low-degree inflammation, insulin resistance and the epidemic of CMD to lower levels of abdominal adiposity. The relative roles played by genetic and environmental factors and the interaction between the two are the still subjects of great debate. We have reviewed the relationship between maternal malnutrition, early growth restriction, epigenetic adaptations, and the later occurrence of abdominal obesity and CMD in Latin America.
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PMID:Epidemic of cardiometabolic diseases: a Latin American point of view. 2140 94

Elevated blood glucose is a major component in metabolic syndrome and pre-diabetes, sometimes leading to type 2 diabetes mellitus (DM II). Additionally, it may lead to adipose deposits when left elevated for long periods. The epidemiology of DM II clearly shows that uncontrolled blood glucose levels leads to many adverse conditions including heart disease, retinal damage, renal failure, erectile dysfunction, and other significant medical conditions. Here we conducted a single-center, prospective, randomized, double-blinded, placebo-controlled, parallel-group- clinical trial of a nutraceutical supplement vs. placebo to measure its glucose lowering effect in generally healthy adults before and after a simple sugars meal. Subjects reported to the test clinic on multiple days to receive placebo or treatment, a simple sugars meal, as well as pre-and postprandial blood glucose measurement (modified oral glucose tolerance test). Each subject served as his or her own control and thirty-one subjects completed the trial with at least one oral glucose tolerance test (OGTT) with the nutraceutical supplement and placebo. Statistical analysis revealed the nutraceutical supplement significantly lowered postprandial glucose levels by 36% and 59% at 45 and 60 minutes, respectively (***P<.001). The study was limited by its composition of primarily overweight females. Future studies will be required over longer periods in more heterogeneous and larger groups to determine the long-term effect of this supplement on blood glucose levels in terms of prophylaxis or treatment for DM II.
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PMID:Evaluation of a novel supplement to reduce blood glucose through the use of a modified oral glucose tolerance test. 2141 63

Urotensin II (UII) binds to its receptor, UT, playing an important role in the heart, kidneys, pancreas, adrenal gland, and central nervous system. In the vasculature, it acts as a potent endothelium-independent vasoconstrictor and endothelium-dependent vasodilator. In disease states, however, this constriction-dilation equilibrium is disrupted. There is an upregulation of the UII system in heart disease, metabolic syndrome, and kidney failure. The increase in UII release and UT expression suggest that UII system may be implicated in the pathology and pathogenesis of these diseases by causing an increase in acyl-coenzyme A:cholesterol acyltransferase-1 (ACAT-1) activity leading to smooth muscle cell proliferation and foam cell infiltration, insulin resistance (DMII), as well as inflammation, high blood pressure, and plaque formation. Recently, UT antagonists such as SB-611812, palosuran, and most recently a piperazino-isoindolinone based antagonist have been developed in the hope of better understanding the UII system and treating its associated diseases.
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PMID:Potential Clinical Implications of the Urotensin II Receptor Antagonists. 2181 63

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