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

This study is to evaluate beta cell function and investigate the mechanism of impaired pancreatic islet beta cell function in monosodium glutamate (MSG) obese rat with insulin resistance, an animal model of metabolic syndrome. Insulin tolerance test was used to screen MSG obese rats with insulin resistance. Blood concentrations of glucose, triglyceride, total cholesterol and insulin were determined. Beta cell function was assessed with hyperglycemic clamp technique. The morphological alterations in pancreas and changes of islet beta cell mass were evaluated by hematoxylin-eosin (HE) and Gomori aldehyde fuchsin staining. Lipid, oxidative stress relevant factors, nitric oxide (NO) level and activity of ATPase in pancreas and pancreatic mitochondrial were tested. The MSG obese rats with insulin resistance could be validated as a typical metabolic syndrome animal model possessing increased fasting plasma triglycerides and insulin (P < 0. 001), markedly decreased weight indices of pancreas and impaired glucose-stimulated insulin secretion. Hematoxylin-eosin (HE) and Gomori aldehyde fuchsin staining showed increased adipocytes and fibroplasia deposition in pancreas and reduced beta cell mass. The increased contents of triglyceride and NO level, the decreased SOD levels and activities of total ATPase (P < 0.001), Na+-K+-ATPase (P < 0.001) and Ca2+-Mg2+-ATPase (P < 0.01) were observed in pancreas and its mitochondria versus normal rat. The study demonstrates that accumulation of lipids in pancreas could lead to increased systemic indicators of inflammation, such as NO, which may influence the activities of several kinds of ATPase in cell membranes and interfere the ion transport, substance metabolism and energy production in pancreas. Finally the MSG obese rats characterized with metabolic syndrome displayed an impairment of beta cell function.
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PMID:[A preliminary study on the mechanism of impaired beta cell function in monosodium glutamate obese rat with insulin resistance]. 1923 28

Arterial hypertension is often part of a constellation of anthropometric and metabolic abnormalities that occur simultaneously to a higher degree than would be expected by chance alone, supporting the existence of a discrete disorder, the so-called metabolic syndrome. It is the result of interactions among a large number of interconnected mechanisms, which eventually lead to both an increase in cardiovascular and renal risk, and the development of diabetes. Mechanisms involved in the metabolic syndrome are obesity, insulin resistance, and a constellation of independent factors, which include molecules of hepatic, vascular, and immunologic origin with pro-inflammatory properties. At each of these key points are interactions of demographics, lifestyle, genetic factors, and environmental fetal programming. Superimposing upon these are infections or chronic exposure or both to certain drugs that can also make their contribution. Skeletal muscle and the liver, not adipose tissue, are the two key insulin-response tissues involved in maintaining glucose balance, although abnormal insulin action in the adipocytes also plays a role in development of the syndrome. Factors commonly associated with and partly dependent on obesity, insulin resistance, such as overactivity of the sympathetic, stimulation of the renin-angiotensin-aldosterone systems, abnormal renal sodium handling, endothelial dysfunction, and large vessels' alterations, may play a key role in the blood pressure elevation of the syndrome.
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PMID:Mechanisms of hypertension in the cardiometabolic syndrome. 1989 34

We have previously reported that peroxynitrite is involved in dysfunction of nitric oxide (NO)-mediated vasorelaxation in SHR/NDmcr-cp rats (SHR-cp), which display typical symptoms of metabolic syndrome. This study investigated whether peroxynitrite is actually generated in the vascular wall with angiotensin II-induced NADPH-oxidase activation, thus contributing to the dysfunction. In isolated mesenteric arteries of male 18-week-old SHR-cp, relaxations in response to acetylcholine and sodium nitroprusside were impaired compared with that in Wistar-Kyoto rats. This impaired relaxation was not restored by treatment with apocynin, an NADPH-oxidase inhibitor. Protein expression of endothelial NO synthase increased while that of soluble guanylyl cyclase (sGC) decreased in the artery. We observed increased production of superoxide anions and peroxynitrite from the artery and their inhibition by apocynin, and also increased contents of nitrotyrosine, a biomarker of peroxynitrite, in mesenteric arteries and angiotensin II in aortas. Long-term (8 weeks) administration of telmisartan, an angiotensin II type 1-receptor antagonist, prevented the impaired vasorelaxation, decreased sGC expression and increased nitrotyrosine content in mesenteric arteries. These findings suggest that in the vascular wall of SHR-cp, peroxynitrite is continually produced by the reaction of NO with NADPH oxidase-derived superoxide via angiotensin II and gradually denatures sGC protein, leading to vasorelaxation dysfunction.
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PMID:Chronic production of peroxynitrite in the vascular wall impairs vasorelaxation function in SHR/NDmcr-cp rats, an animal model of metabolic syndrome. 1934 75

The mechanism underlying blood pressure (BP) reduction in the high fruits and vegetables arm of the Dietary Approaches to Stop Hypertension (DASH) study is unknown but may include potassium, magnesium and fibre. This study was designed to separate minerals and fibre from other components of DASH on BP in abdominally obese individuals with metabolic syndrome with pre-hypertension to stage 1 hypertension (obese hypertensives). A total of 15 obese hypertensives and 15 lean normotensives were studied on a standardized usual diet, randomized to DASH or usual diet supplemented with potassium, magnesium and fibre to match DASH, then crossed over to the complementary diet. All diets were 3 weeks long, isocaloric and matched for sodium and calcium. In obese hypertensives, BP was lower after 3 weeks on DASH than usual diet (-7.6+/-1.4/-5.3+/-1.4 mm Hg, P<0.001/0.02) and usual diet supplemented (-6.2+/-1.4/-3.7+/-1.4 P<0.005/0.06), whereas BP was not significantly different on usual and supplemented diets. BP values were not different among the three diets in lean normotensives. Small artery elasticity was lower in obese hypertensives than in lean normotensives on the usual and supplemented diets (P<0.02). This index of endothelial function improved in obese hypertensives (P<0.02) but not lean normotensives on DASH, and was no longer different from values in lean normotensives (P>0.50). DASH is more effective than potassium, magnesium and fibre supplements for lowering BP in obese hypertensives, which suggest that high fruits and vegetables DASH lowers BP and improves endothelial function in this group by nutritional factors in addition to potassium, magnesium and fibre.
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PMID:DASH lowers blood pressure in obese hypertensives beyond potassium, magnesium and fibre. 1962 43

One main pathophysiological mechanism underlying the increased risk for uric acid nephrolithiasis in humans with the metabolic syndrome is the excretion of unduly acidic urine, in part because of reduced excretion of the main urinary buffer, ammonium. The Zucker diabetic fatty (ZDF) rat, an established rodent model of the metabolic syndrome, has similar urinary abnormalities, attributed in part to lower expression and activity of the principal mediator of proximal tubule ammonium excretion, brush-border membrane Na+/H+ exchanger 3 (NHE3). These defects are associated with renal tubular steatosis in ZDF rats, but the causal relationship between renal steatosis and defective urinary acidification has not been investigated in vivo. We hypothesized that reduction of renal steatosis would commensurately normalize urinary acidification parameters. We treated ZDF rats with thiazolidinediones to reduce nonadipose tissue steatosis. Four weeks of treatment reduced renal triglyceride accumulation and restored urinary acidification parameters in ZDF rats to levels comparable to their lean littermates; urinary acidification was not affected by treatment in lean rats. To further document the direct effects of fat, we showed that functional abnormalities induced by fat loading in a cell culture model of proximal tubule steatosis and lipotoxicity can be reversed by fat removal but not by thiazolidinediones alone. Together, these findings support the causative role of renal steatosis in the pathogenesis of urinary acidification defects, demonstrate reversibility upon lipid removal, and highlight a potential therapeutic strategy for renal abnormalities in the metabolic syndrome.
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PMID:Reduction of renal triglyceride accumulation: effects on proximal tubule Na+/H+ exchange and urinary acidification. 1969 86

The objective of this study was to investigate the association between sodium intake and metabolic syndrome (MS) in individuals free from the confounding effects of increased blood pressure (BP). In all, a total of 1655 individuals (45.8% men) who participated in the MONICA-WHO/Vitoria Project, mean age 45+/-11 years were investigated. According to NCEP-ATP lll criteria, MS prevalence was 32.9 and 85% of these individuals had BP >130/85 mm Hg. Thus, high BP represents the main MS risk factor. Twelve-hour nocturnal urine (1900 to 0700 hours) was used to measure urinary sodium and potassium excretion. Sodium excretion was associated with BP. From the optimal BP level up to stage lll hypertension, the mean (median) sodium excretion increased from 99 (89) to 128 (134) mEq and from 81 (69) to 112 (103) mEq in men and women, respectively (P<0.001 for trend; median). However, when 781 individuals with BP <130/85 mm Hg (including 80 drug-free normotensive individuals with MS) were stratified according to the gender and number of MS components, no significant differences were observed either in the urinary volume or in the sodium or potassium excretion. For each of the four MS components, sodium excretion was 96+/-48, 97+/-53, 108+/-65 and 97+/-49 mEq for men, and 83+/-51, 83+/-58, 80+/-49 and 93+/-45 mEq for women, respectively. No differences were found in urinary sodium excretion in normotensive individuals, regardless of the presence of MS. Therefore, it seems that high sodium intake is not an MS predictor per se as suggested earlier.
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PMID:Salt excretion in normotensive individuals with metabolic syndrome: a population-based study. 1969 79

This study included 49 patients with coronary heart disease (CHD) and arterial hypertension (AH) in whom comprehensive medical examination revealed metabolic syndrome (MA). The objective of the work was to ascertain the possibility of therapy courses using chloride-hydrocarbonate-sodium mineral water and to evaluate its corrective effect on metabolic processes and functional disturbances of the biliary tract. It was shown that mineral water has beneficial effect in patients with functional incompetence of the biliary tract. Elimination of pain syndrome and resolution of dyspeptic symptoms was associated with the improvement of physico-chemical characteristics of the bile in the majority of the patients. These changes developed 1.5-2 times sooner than in the absence of therapy which substantially improved quality of life of the patients. Another positive result of mineral water consumption was the reduced level of blood lipids, in the first place that of total cholesterol and triglycerides. The efficiency of corrective action of non-medicamentous treatment modalities, such as courses of intake of chloride-hydrocarbonate-sodium mineral water, in patients with functional disturbances of the biliary tract is comparable with that of recommended drug therapy. The hypolipidemic effect of chloride-hydrocarbonate-sodium mineral water demonstrated in the present study allows it to be recommended as a tool for non-medicamentous correction of hyperlipidemia known to be not only a risk factor of CHD and AH but also as a constituent component of metabolic syndrome. The data obtained suggest the possibility to improve efficiency of the treatment of motor dysfunction of the biliary tract and metabolic disorders inherent in metabolic syndrome.
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PMID:[Non-medicamentous correction of metabolic and functional disorders in the biliary tract of patients with metabolic syndrome]. 1970 61

Recent studies have shown that sodium intake restrictions may increase insulin resistance (IR) and induce changes on serum lipoproteins and on inflammation markers that are similar to those found in metabolic syndrome (MS). We performed a systematic review of literature regarding the effects of restricting sodium intake on MS or on IR. Nine articles were included in the review. Restriction of sodium consumption was associated with increase insulin resistance in two articles and with decrease in three others. In seven of nine articles, salt intake restriction determined blood pressure reduction, and in two articles adverse effects on markers of MS were found. Most studies showed beneficial effects of moderate sodium intake restriction, associated or not to others nutritional modifications or increased physical activity. Further studies are needed to evaluate the effects of moderate sodium consumption reductions on MS and IR.
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PMID:[Sodium intake and metabolic syndrome: a systematic review]. 1976 51

Obesity is associated with endothelial dysfunction related to decreased NO bioavailability, increased endothelin 1 vasoconstrictor activity, and decreased circulating ghrelin. Therefore, we tested whether exogenous ghrelin may have benefits to improve the balance between endothelin 1 and NO in patients with obesity-related metabolic syndrome. Vasoactive actions of endothelin 1 and NO were assessed in 8 patients with metabolic syndrome and 8 matched controls by evaluating forearm blood flow responses (strain-gauge plethysmography) to intra-arterial infusion of BQ-123 (endothelin A receptor antagonist; 10 nmol/min), followed by NG-monomethyl-L-arginine (NO synthase inhibitor; 4 micromol/min), before and after infusion of ghrelin (200 ng/min). In the absence of ghrelin, the vasodilator response to BQ-123 was greater in patients than in controls (P<0.001), whereas infusion of NG-monomethyl-L-arginine induced smaller vasoconstriction in patients than in controls (P=0.006). Importantly, exogenous ghrelin decreased the vasodilator response to BQ-123 (P=0.007 versus saline) and enhanced the magnitude of changes in forearm blood flow induced by NG-monomethyl-L-arginine (P=0.003) in patients but not in controls (both P>0.05). The favorable effect of ghrelin on endothelin A-dependent vasoconstriction was likely related to the stimulation of NO production, because no change in the vascular effect of BQ-123 was observed after ghrelin (P=0.44) in 5 patients with metabolic syndrome during continuous infusion of the NO donor sodium nitroprusside (0.2 microg/min). In patients with metabolic syndrome, ghrelin has benefits to normalize the balance between vasoconstrictor (endothelin 1) and vasodilating (NO) mediators, thus suggesting that this peptide has important peripheral actions to preserve vascular homeostasis in humans.
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PMID:Ghrelin restores the endothelin 1/nitric oxide balance in patients with obesity-related metabolic syndrome. 1978 44

Through its classic effects on sodium and potassium homeostasis, aldosterone, when produced in excess, is associated with the development of hypertension and hence with higher cardiovascular and renal risk. In recent years, experimental and epidemiologic data have suggested that aldosterone also may be linked to high cardiovascular risk independently of its effects on blood pressure. Thus, aldosterone has been associated with obesity and metabolic syndrome in selected populations, and these associations may further contribute to the higher cardiovascular risk of subjects with elevated aldosterone levels. Moreover, aldosterone has been reported to promote inflammation, oxidative stress, and fibrosis in a number of tissues. Clinical evidence indicates that patients with primary hyperaldosteronism have a higher risk of developing cardiovascular and renal complications than patients with essential hypertension who have the same level of blood pressure. Aldosterone receptor blockade has been shown to lower cardiovascular mortality after myocardial infarction and in patients with congestive heart failure. Some studies have also demonstrated that aldosterone blockade could have a favorable impact on the progression of renal disease. However, prospective interventional trials are needed to further evaluate the impact of blockade of aldosterone on cardiovascular risk.
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PMID:Aldosterone and cardiovascular risk. 1989 57


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