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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nonalcoholic fatty liver (NAFL) is a common comorbidity in patients with type 2 diabetes and links to the risk of coronary syndromes. The aim was to determine the manifestations of metabolic syndrome in different organs in patients with liver steatosis. We studied 55 type 2 diabetic patients with coronary artery disease using positron emission tomography. Myocardial perfusion was measured with [15O]H2O and myocardial and skeletal muscle glucose uptake with 2-deoxy-2-[18F]fluoro-D-glucose during hyperinsulinemic euglycemia. Liver fat content was determined by magnetic resonance proton spectroscopy. Patients were divided on the basis of their median (8%) into two groups with low (4.6 +/- 2.0%) and high (17.4 +/- 8.0%) liver fat content. The groups were well matched for age, BMI, and fasting plasma glucose. In addition to insulin resistance at the whole body level (P = 0.012) and muscle (P = 0.002), the high liver fat group had lower insulin-stimulated myocardial glucose uptake (P = 0.040) and glucose extraction rate (P = 0.0006) compared with the low liver fat group. In multiple regression analysis, liver fat content was the most significant explanatory variable for myocardial insulin resistance. In addition, the high liver fat group had increased concentrations of high sensitivity C-reactive protein, soluble forms of E-selectin, vascular adhesion protein-1, and intercellular adhesion molecule-1 (P < 0.05) and lower coronary flow reserve (P = 0.02) compared with the low liver fat group. In conclusion, in patients with type 2 diabetes and coronary artery disease, liver fat content is a novel independent indicator of myocardial insulin resistance and reduced coronary functional capacity. Further studies will reveal the effect of hepatic fat reduction on myocardial metabolism and coronary function.
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PMID:Liver steatosis coexists with myocardial insulin resistance and coronary dysfunction in patients with type 2 diabetes. 1647 72

The aim of the present study was to determine the accuracy of reported energy intake according to a food-frequency questionnaire (FFQ) and dietary records (DR) in obese subjects with metabolic syndrome risk factors. Subjects were twenty-three men and twenty-seven women with mean BMI of 35.7 (range 30.5-43.8) kg/m(2) who participated in a dietary interview based on a FFQ and completed weighed DR. Total energy expenditure was measured with the doubly labelled water method. Total energy expenditure, measured RMR and physical activity level did not differ between under-reporters (50 % of the sample) and non-under-reporters. Under-reporters had lower median intake of sweets, desserts and snacks than non-under-reporters (100 v. 161 g/d (P = 0.0008) and 61 v. 128 g/d (P = 0.0002) according to the FFQ and DR, respectively). The DR also showed lower energy density (6.7 (sd 1.3) v. 7.9 (SD 1.6) kJ/g; P = 0.0064), lower intake of sugary drinks (0 v. 167 g/d; P = 0.0063) and higher scores for dietary restraint (9.0 (sd 5.0) v. 6.1 (SD 3.5); P = 0.0285) in under-reporters. Energy density was associated with accuracy according to the FFQ (Spearman's rank correlation coefficient (RS) 0.406; P = 0.0034) and the DR (RS 0.537; P < 0.0001). In multivariate analysis, consumption of bread and sweets, desserts and snacks measured by the FFQ was positively associated with accuracy (R(2)adjusted 0.46 (95 % CI 0.32, 0.70)). According to the DR, consumption of sweets, desserts and snacks was also associated with accuracy, as was dietary restraint (inversely) (R(2)adjusted 0.67 (95 % CI 0.54, 0.83)). In obese subjects with metabolic risk factors, intake of sweets, desserts and snacks, bread and dietary restraint were determinants of reporting accuracy.
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PMID:Accuracy of food intake reporting in obese subjects with metabolic risk factors. 1651 51

Sucrose-fed rats (HTG) develop hypertension, hypertriglyceridemia, and other features of the metabolic syndrome. This condition, nowadays a world epidemic, is more prevalent in males and increases the risk of cardiovascular diseases. Weanling male and female rats were given either tap water in control (C) or 30% sucrose solution in HTG groups and commercial rat chow for 3, 5, or 8 months. We studied possible variations in cardiac function, due to gender and length of treatment, in isolated heart after ischemia-reperfusion, since an impaired performance may be more easily detected under stress. Together, sucrose treatment and age affected all cardiac variables. Gender had significant effect on coronary vascular resistance and postischemic levels of the enzyme CK-MB; the percentages of retained cardiac enzymes after ischemia were higher in C and HTG females. C and HTG males had a higher incidence of arrhythmias than females, but only HTG males suffered lethal ventricular fibrillation.
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PMID:Isolated heart function after ischemia and reperfusion in sucrose-fed rats: influence of gender and treatment. 1654 36

Obesity is frequently accompanied by insulin resistance, type II diabetes, hypertension and atherosclerosis, a cluster of pathologies that are the major components of the metabolic syndrome. Obesity is a known cause for renal dysfunction that leads to two major renal pathologies: hypertension and glomerular and tubulointerstitial injury. Peroxizome proliferator activated receptors (PPARs) are transcription factors belonging to the nuclear hormone receptor superfamily with important functions in the regulation of metabolism. The role of PPARgamma isoforms in adipogenesis and vascular inflammation associated to obesity has been vastly studied and is well recognized, albeit not completely mechanistically understood. Also, the effect of various PPARgamma agonists on blood pressure reduction in different forms of hypertension, including obesity related hypertension has been reported, but the mechanisms involved are only beginning to be studied. Even less clear is the concurrent beneficial effect of PPARgamma agonists thiazolinendiones (TZD) on blood pressure reduction in different forms of hypertension and, at the same time, in some cases, the significant water retention leading to edema and heart failure. The occurrence of both these apparently opposite effects on the renal water and sodium handling suggests a complex role of PPARgamma in the kidney that is likely related to the metabolic state. Also, PPARgamma activation leads to a reduction in mesangial cell proliferation while stimulating apoptosis. TZD treatment reduces albuminuria in obese and diabetic humans and rodent models suggesting protective effects against renal tubuloglomerular injury. The focus of this review is to present and critically discuss the recent findings on the roles of PPARgamma in the kidney in direct relation to renal function and renal injury in obesity and obesity-initiated diabetes.
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PMID:The complex role of PPARgamma in renal dysfunction in obesity: managing a Janus-faced receptor. 1671 56

The aim of the present study was to clarify the effect of telmisartan, an angiotensin II receptor blocker, on the development of obesity and related metabolic disorders in diet-induced obese mice. Treatment with telmisartan dissolved in drinking water at a dosage of 5 mg/kg per day for 14 days attenuated the diet-induced weight gain without affecting food intake in diet-induced obese mice compared with controls using nontreated water. Telmisartan treatment decreased the weight of visceral adipose tissue and the triglyceride content in the liver and skeletal muscle. In addition, hyperglycemia, hyperinsulinemia, and hypertriglyceridemia in diet-induced obese mice all improved with telmisartan treatment. Furthermore, telmisartan treatment increased adiponectin mRNA in visceral white adipose tissue and was associated with a concomitant change in the serum adiponectin level. In contrast, the treatment reduced the serum level of resistin. Finally, telmisartan treatment increased the mRNA expression of uncoupling protein 1 in brown adipose tissue and was accompanied by an increase in oxygen consumption. In conclusion, telmisartan treatment might prevent the development of obesity and related metabolic disorders by altering the levels of adiponectin, resistin, and uncoupling protein 1 in diet-induced obese mice. Our results indicate that telmisartan can be used as a therapeutic tool for metabolic syndrome, including visceral obesity.
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PMID:Telmisartan prevents obesity and increases the expression of uncoupling protein 1 in diet-induced obese mice. 1671 45

beta3-Adrenoreceptor agonists can stimulate lipolysis in the white adipose tissue and thermogenesis in the brown adipose tissue. These activities could be useful in the treatment of obesity and the associated metabolic syndrome. The effects of six-week oral administration of the newly synthesized substance B496 (methyl-4-[2-[2-hydroxy-3-(4-ethylcarbamoyl)phenoxyprophyl]amino]etyl)-phenoxyacetate hydrochloride) on serum glucose, triglycerides, total cholesterol, and leptin levels were studied in male Wistar rats fed with a high-fat diet. The animals were divided into a group treated with B496 (5 mg dissolved in 1 litre of water) and a control group. The results indicated a significant reduction in serum glucose levels (-26 %, p<0,01), triacylglyceride levels (-21 %, p<0,05) and leptin levels (-43 %, p<0,01). Further the effect of a single intraperitoneal dose (1 mg/kg) of B496 and BRL-37344 on serum leptin levels in the C57Bl/6J mouse was investigated. Administration of BRL-37344 resulted in a significant decrease in serum leptin levels (-55 %, p<0,001). This reduction was not demonstrated by newly synthesized substance B496.
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PMID:[Study of a newly synthesized substance with a potential to stimulate beta3-adrenergic receptors]. 1683 89

Fructose intake has been recently linked to the epidemic of metabolic syndrome and, in turn, the metabolic syndrome has been epidemiologically linked with renal progression. The renal hemodynamic effects of fructose intake are unknown, as well as the effects of different routes of administration. Metabolic syndrome was induced in rats over 8 wk by either a high-fructose diet (60%, F60, n = 7) or by adding fructose to drinking water (10%, F10, n = 7). Body weight and food and fluid intake of each rat were measured weekly during the follow-up. At baseline and at the end of wk 8, systolic blood pressure, plasma uric acid, and triglycerides were measured. At the end of week 8 glomerular hemodynamics was evaluated by micropuncture techniques. Wall thickening in outer cortical and juxtamedullary afferent arterioles was assessed by immunohistochemistry and computer image analysis. Fructose administration either in diet or drinking water induced hypertension, hyperuricemia, and hypertriglyceridemia; however, there was a progressive increment in these parameters with higher fructose intake (C<F10<F60). In addition, the F60 rats developed kidney hypertrophy, glomerular hypertension, cortical vasoconstriction, and arteriolopathy of preglomerular vessels. In conclusion, fructose-induced metabolic syndrome is associated with renal disturbances characterized by renal hypertrophy, arteriolopathy, glomerular hypertension, and cortical vasoconstriction. These changes are best observed in rats administered high doses (60% diet) of fructose.
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PMID:Fructose-induced metabolic syndrome is associated with glomerular hypertension and renal microvascular damage in rats. 1694 May 62

The Zucker obese rat is an important model for the metabolic syndrome, which includes renal disease and salt-sensitive hypertension, suggesting abnormalities of body fluid regulation. Here, in Zucker rats, lean and obese, and of both sexes, we compared 48 h of sodium intake and fluid regulation responses with repeated depletions with furosemide to repeated control saline injections. Increased urine volume excretion was observed after each furosemide administration for the 4 groups and obese rats excreted more than the leans on the control days. Male obese rats did not excrete sodium nor increase intake of 2% NaCl following the first furosemide administration, whereas the other 3 groups did. Subsequent depletions increased 2% NaCl consumption and urinary sodium excretion in all groups. Males excreted more sodium in their urine than the females on the control days. Females showed an increase in 2% NaCl intake on control days. Water intake increased in the female leans after each depletion, increased in the males after the 2nd and 3rd depletion and increased in the obese females only after the 2nd depletion. These findings show clearly that there are gender- and weight-related differences in the response of Zucker rats to furosemide-induced depletion. However, the main differences occurred with the first depletion. With repeated depletions the rats adjusted sodium and fluid intake and excretion so that differences due to gender and body weight tended to disappear. Our findings caution against drawing conclusions about differences due to gender and body weight based on single treatments.
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PMID:Gender and obesity influence sodium intake and fluid regulation in Zucker rats following repeated sodium depletions. 1695 27

Antipsychotic drugs induce weight gain and metabolic abnormalities. Recently, the role of adipocytokines secreted from adipocytes in the development of metabolic syndrome has received attention. The aim of this study was to investigate the effects of chlorpromazine (Cp) on body weight, glucose, lipid metabolism, and adipocytokine secretion in rats fed sucrose. Wistar rats received 15% sucrose (Suc group), 15% sucrose and Cp at 7.5 mg/kg per day (Suc + Cp group), or Cp alone (Cp group) in water for 10 weeks. Fasting glucose levels in the Suc and Suc + Cp groups were significantly higher than in the control (Cont) group. Fasting insulin levels in the Suc, Suc + Cp, and Cp groups were also significantly higher than in the Cont group. The adiponectin level in the Suc group was significantly higher than in the Cont group, although the adiponectin level in the Suc + Cp group was not. Furthermore, the plasma tumor necrosis factor (TNF)-alpha level in the Suc + Cp group was significantly higher than in the Suc group. These data suggest that Cp inhibits the compensatory response of adiponectin with respect to obesity due to increased expression of plasma TNF-alpha level. Cp may exert more harmful effects on the glucose level and insulin resistance than on other factors, which may be one of the mechanisms responsible for the metabolic syndrome induced by antipsychotic agents.
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PMID:The elucidation of the mechanism of weight gain and glucose tolerance abnormalities induced by chlorpromazine. 1703 Oct 68

In spite of a progressive fall in the incidence of traditional risk factors of cardiovascular morbidity (cigarette smoking, high blood pressure, and hyperlipidemia), there is an upward trend in the prevalence of obesity and chronic kidney disease (CKD). Furthermore, there is a strong correlation between body mass indices and the relative risk of progression of CKD. The close biophysiological interaction between obesity and CKD is evident by a similar occurrence of comorbidities including insulin resistance, hyperlipidermia, endothelial dysfunction, and sleep disorders. Truncal obesity is a primary component of metabolic syndrome; unlike peripheral fat, the visceral adipocytes are more resistant to insulin. In addition, lipolysis results in a release of free fatty acid and TG, whereas hypertriglycedemia is potentiated by uremic activation of fatty acid synthase. Hypertriglycedemia and low HDL cholesterol increase the relative risk of progression of CKD. Furthermore, endothelial inflammation and premature atherosclerosis are promoted by hyperhomocysteinemia and oxidation of LDL, both of which are commonly observed in CKD and obesity. Predominance of oxidative stress in both obesity and azotemia stimulate synthesis of angiotensin II, which in turn increases TGF-B and plasminogen activator inhibitor-1, thereby propagating glomerular fibrosis. Furthermore, local synthesis of angiotensinogen by adipocytes, leptin activation of sympathetic nervous system, and hyperinsulinemia contribute to the development of hypertension in obesity and CKD. In addition, increased renal tubular expression of Na-K-ATPase and a blunted response to natiuretic hormones in obesity promote salt and water retention. Glomerular hyperfiltration from systemic volume load and hypertension results in mesangial cellular proliferation and progressive renal fibrosis. In addition, maternal nutritional deprivation increases the incidence of obesity, hypertension, and diabetes in adulthood. Reduced fetal protein synthesis contributes to oxidative glomerular injury and impairment of renal morphogenesis. Thus, kidneys are poorly equipped to handle physiologic stress that may result from the rapid body growth and programmed metabolic dysfunction later in life. Finally, in order to minimize morbidity of obesity-related kidney disease, preventive strategy must include optimal maternal health care, promotion of healthy nutrition and routine physical exercise, and early detection of CKD.
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PMID:The role of obesity and its bioclinical correlates in the progression of chronic kidney disease. 1704 21


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