Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Elevated circulating ADMA levels have been proposed as the pivotal link between insulin resistance, cardiovascular disease, and endothelial dysfunction in Caucasian population. To evaluate whether there is an association between plasma ADMA concentrations and insulin resistance in Hispanic population, we identified metabolic syndrome NCEP-ATP III criteria and measured ADMA and L-arginine plasma concentrations in 147 Colombian young males consecutively included in a cross-sectional study. In contrast to inflammatory markers, ADMA was not found to be elevated in subjects with metabolic syndrome, furthermore, no significant association between ADMA concentrations and insulin resistance degree was found. In conclusion, our results suggest that at least in our population, ADMA does not seem to be implicated in the pathophysiology of metabolic syndrome. Ethnic-specific or environmental differences in the etiologic mechanisms of metabolic syndrome need to be elucidated in further studies.
 ...
PMID:Plasma concentrations of asymmetric dimethylarginine (ADMA) in metabolic syndrome. 1723 81

Coronary artery disease (CAD) is the leading cause of death worldwide and is commonly caused by a constellation of risk factors called the metabolic syndrome. We characterized a family with autosomal dominant early CAD, features of the metabolic syndrome (hyperlipidemia, hypertension, and diabetes), and osteoporosis. These traits showed genetic linkage to a short segment of chromosome 12p, in which we identified a missense mutation in LRP6, which encodes a co-receptor in the Wnt signaling pathway. The mutation, which substitutes cysteine for arginine at a highly conserved residue of an epidermal growth factor-like domain, impairs Wnt signaling in vitro. These results link a single gene defect in Wnt signaling to CAD and multiple cardiovascular risk factors.
 ...
PMID:LRP6 mutation in a family with early coronary disease and metabolic risk factors. 1733 14

Modulation by sex hormones of aortic reactivity in rats with the metabolic syndrome (MS) was investigated. The following groups of weanling male Wistar rats were used: control rats (C) received regular tap water while MS rats received 30% sucrose in their drinking water; both had rodent chow for 24 weeks. These two groups were further subdivided into the following four groups: intact (Int), castrated (Cas), castrated plus testosterone (T) and castrated plus estradiol (E). Vascular response of thoracic aortic rings to norepinephrine (NE), acetylcholine (ACh), indomethacin (Indo) and nitro-l-arginine-methyl ester (L-NAME) was investigated. Blood pressure (BP) and serum nitrates and nitrites were measured. BP and serum nitrates and nitrites were modified by castration and treatments with either T or E. Vasoconstriction in Int MS and Cas MS+T aortas was larger than in C and Cas C+T, respectively. Vasodilation in Int MS and Cas MS+T was reduced in comparison with C and Cas C+T, Cas MS and Cas MS+E. Indomethacin decreased vasoconstriction in all groups (P<0.002) but Int C and Cas C+T remained significantly smaller than Int MS and Cas MS+T. l-NAME in NE-contracted vessels induced a significant increase in vasoconstriction, except in Cas C+E rats; the responses of Int MS and Cas MS+T were significantly larger than in Int C and Cas C+T. The results suggest endothelial dysfunction in Int MS and Cas MS+T and a protective effect resulting from castration and castration plus E in MS animals, indicating a sex hormone influence.
 ...
PMID:Modulation of aortic vascular reactivity by sex hormones in a male rat model of metabolic syndrome. 1749 11

Chronic increases in blood flow increase arterial diameter and NO-dependent dilation in resistance arteries. Because endothelial dysfunction accompanies metabolic syndrome, we hypothesized that flow-mediated remodeling might be impaired in obese rat resistance arteries. Obese and lean Zucker rat mesenteric resistance arteries were exposed to chronic flow increases through arterial ligation in vivo: arteries exposed to high flow were compared with normal flow arteries. Diameter was measured in vitro in cannulated arteries using pressure arteriography. After 7 days, outward remodeling (diameter increased from 346+/-9 to 412+/-11 mum at 100 mm Hg) occurred in lean high-flow arteries. Endothelium-dependent tone was reduced in high-flow arteries from obese rats by contrast with lean animals. On the other hand, diameter enlargement occurred similarly in the 2 strains. The involvement of NO in endothelium-dependent dilation (evidenced by NO blockade) and endothelial NO synthase phosphorylation was smaller in obese than in lean rats. Superoxide anion and reduced nicotinamide-adenine dinucleotide phosphate oxidase subunit expression (p67phox and gp91phox) increased in obese rats and were higher in high-flow than in control arteries. Acute Tempol (a catalase mimetic), catalase plus superoxide dismutase, and l-arginine plus tetrahydrobiopterin restored endothelium-dependent dilation in obese rat normal and high-flow arteries to the level found in lean control arteries. Thus, flow-induced remodeling in obese resistance arteries was associated with a reduced endothelium-mediated dilation because of a decreased NO bioavailability and an excessive superoxide production. This dysfunction might have negative consequences in ischemic diseases in patients with obesity or metabolic syndrome.
 ...
PMID:Flow-induced remodeling in resistance arteries from obese Zucker rats is associated with endothelial dysfunction. 1751 52

The aim was to evaluate whether the metabolic syndrome associates with other endocrinopathies observed after allogeneic stem cell transplantation (SCT) in childhood. Thirty-one SCT long-term survivors, transplanted for leukemia (n=26) or nonmalignant hematologic diseases (n=5) were evaluated by oral glucose tolerance test and assessment of serum lipids at a median age of 15 (range 7 to 34) years. Hyperinsulinemia, hypertriglyceridemia, and abdominal obesity were required for the diagnosis of metabolic syndrome. Growth hormone (GH) secretion was evaluated either with GH releasing hormone and arginine (n=14), clonidine (n=15), or insulin-tolerance (n=2) test. A GH peak level of <20 mU/L was considered insufficient. The thyroid and gonadal functions were assessed. Twelve patients (39%) had metabolic syndrome. Nine out of 12 (75%) patients with metabolic syndrome had insufficient GH response in provocative testing as opposed to 6/19 (31%) of those without it (P=0.02). No difference was observed in thyroid or gonadal function between patients with versus without metabolic syndrome. In conclusion, metabolic syndrome is frequently associated with insufficient GH secretion in the SCT long-term survivors. This should implicate a close follow-up of the metabolic parameters in SCT patients with either frank GH insufficiency or signs of inadequate GH response in provocative testing.
 ...
PMID:Insufficient growth hormone secretion is associated with metabolic syndrome after allogeneic stem cell transplantation in childhood. 1776 93

Increased arterial stiffness is influenced by both functional and structural properties of the vessel wall, including changes in content of smooth muscle, elastin and collagen, reduced endothelial production of NO and increased release of endothelin-1 or AngII (angiotensin II). The RAS (renin-angiotensin) system is likely to be central to increases in arterial stiffness, since the changes in arterial structure observed with enhanced AngII activity are similar to the same pathophysiological changes that contribute to arterial stiffness. The role of AT(1)R and AT(2)R (AngII type 1 and type 2 receptors respectively) in the development of arterial stiffening, particularly in the early stages of insulin resistance, is however unclear. In this issue of Clinical Science, Brillante and co-workers have observed that in insulin-resistant subjects exhibiting reduced arterial stiffness, wave reflection from small-to-medium-sized, but not large, arteries was increased following separate intravenous infusions of AngII, the selective AT(2)R inhibitor PD123319 and the NO inhibitor L-NMMA (N(G)-monomethyl-L-arginine) in comparison with normal healthy age- and sex-matched controls. These increases probably reflect increased AT(1)R and AT(2)R expression/activity in addition to up-regulation of basal NO release in the small-to-medium-sized arteries. These changes may be compensatory mechanisms related to early vascular damage and may have clinical implications for treatment in hypertensive patients with evidence of the metabolic syndrome.
 ...
PMID:Does compensatory nitric oxide and angiotensin II receptor activity reduce arterial stiffness in early-stage insulin resistance? 1768 97

Insulin resistance is a major contributor to macro- and microvascular complications, particularly in the presence of the metabolic syndrome, and is also associated with polycystic ovary syndrome. Impaired nitric oxide metabolism and endothelial function are important components of the vascular disease. Increasing the bioavailability of arginine, the precursor of nitric oxide, thus potentially offers protection against end-stage disease. We have recently demonstrated that dietary supplementation with a novel silicate inositol arginine complex reduces vasculopathy and glomerular sclerosis in the insulin-resistant JCR:LA-cp rat. The objective of this study was to address the absorption of, and the underlying metabolic alterations caused by, the arginine silicate inositol complex and arginine HCl (as a reference agent) in obese insulin-resistant male and female JCR:LA-cp rats. Male and female rats were treated with the preparations at 1.0 mg/(kg d) (expressed as arginine HCl) from 8 to 12 and 12 to 18 weeks of age, respectively. Obese female, but not male, rats treated with the arginine silicate inositol complex showed a reduced rate of weight gain without concomitant reduction in food intake. Plasma silicon levels were raised very significantly in arginine silicate-treated rats, consistent with significant absorption of the complex. In male rats, arginine levels were elevated by treatment with arginine silicate only; and female rats responded to both preparations. Plasma concentrations of oxides of nitrogen in rats treated with the silicate complex showed a dimorphism, decreasing in male and increasing in female rats. Fasting insulin levels were elevated in male rats treated with the arginine silicate complex, whereas fasting and postprandial insulin levels were decreased in female rats. Furthermore, female, but not male, rats treated with either of the arginine preparations showed significant reductions in cholesterol, triglyceride, and phospholipid concentrations. We conclude that the arginine silicate inositol complex is absorbed efficiently, raising plasma arginine levels, and is more biologically effective than the free amino acid hydrochloride. This has different beneficial metabolic effects in both sexes of an animal model of insulin resistance and cardiovascular disease, consistent with reduction in end-stage disease.
 ...
PMID:Metabolic effects of a novel silicate inositol complex of the nitric oxide precursor arginine in the obese insulin-resistant JCR:LA-cp rat. 1788 39

We examined oxidative stress and metabolic characteristics of the spontaneously hypertensive hyperlipidemic rat (SHHR) when it was fed a high-fat diet and sucrose solution (HFDS) after N(G)-nitro-L-arginine methyl ester ingestion to develop a rat model of metabolic syndrome. This study was carried out to assess the effects of pioglitazone on levels of lipid peroxide (LPO), Cu,Zn superoxide dismutase (Cu,Zn-SOD), catalase (CAT), glutathione peroxidase (GPx), and non-esterified fatty acids (NEFA) in the plasma and liver tissue in HFDS-SHHR compared with Sprague-Dawley rats (SD). In the HFDS-treated groups, levels of LPO, CAT, GPx, and NEFA were elevated and levels of Cu,Zn-SOD were reduced in the plasma and liver tissue, with a marked accumulation of visceral fat. The changes induced by HFDS feeding were severe in the SHHR model that had essential hypertension and hyperlipidemia, when compared with SD that did not have these essential risk factors. Subcutaneous injection of 10 mg/kg per day of pioglitazone for 2 months significantly restored levels of LPO, CAT, GPx, Cu,Zn-SOD, and NEFA in the HFDS-SHHR group, and visceral fat accumulation was reduced. These results suggest that HFDS-SHHR is a suitable model of metabolic syndrome and that pioglitazone treatment can improve oxidative dysregulation in this rat model.
 ...
PMID:Effects of pioglitazone on increases in visceral fat accumulation and oxidative stress in spontaneously hypertensive hyperlipidemic rats fed a high-fat diet and sucrose solution. 1791 67

The prostaglandin E synthase 2 (PTGES2) gene maps to a locus linked to obesity and is involved in the synthesis of the antilipolytic compound prostaglandin E(2). In a recent study, we found an association of the minor PTGES2 Arg298His allele and lower risk of type 2 diabetes mellitus in the European Investigation into Cancer and Nutrition (EPIC) and Cooperative Health Research in the Augsburg Region (KORA) cohorts. Here, we employed our Metabolic Intervention Cohort Kiel (MICK) to assess the influence of the PTGES2 Arg298His polymorphism on a wider scale of parameters of the metabolic syndrome and postprandial metabolism. In comparison to subjects homozygous for the Arg allele, carriers of the His-allele showed significantly lower fasting insulin (geometric mean +/- SEM: 11.8 muU/mL, 11.41-12.25 versus 13.0, 12.71-13.33; p = 0.023), lower postprandial insulin levels after an oral glucose tolerance test (area under the curve 77.2, 74.07-80.52 versus 81.2, 78.8-83.63; p = 0.023) and lower homeostasis model assessment (HOMA)-insulin-resistance (3.030, 2.909-3.157 versus 3.346, 3.257-3.438; p = 0.041) and HOMA-beta-cell-function (107.2, 104.04-110.52 versus 117.2, 114.65-119.71; p = 0.019). Adjustment for body mass index (BMI) resulted in a loss of these significant differences. BMI tended to show lower values in His-allele carriers, (p = 0.067). In conclusion, risk-reducing effects of the minor His allele of the PTGES2 Arg298His polymorphism could be mediated partly by lowered BMI.
 ...
PMID:Prostaglandin E synthase 2 (PTGES2) Arg298His polymorphism and parameters of the metabolic syndrome. 1797 97

Watermelon is rich in L-citrulline, an effective precursor of L-arginine. This study was conducted to determine whether dietary supplementation with watermelon pomace juice could ameliorate the metabolic syndrome in the Zucker diabetic fatty (ZDF) rat, an animal model of noninsulin-dependent diabetes mellitus. Nine-week-old ZDF rats were assigned randomly to receive drinking water containing 0% (control) or 0.2% L-arginine (as 0.24% L-arginine-HCl), 63% watermelon pomace juice, 0.01% lycopene, or 0.05% citrus pectin (n = 6 per treatment). At the end of the 4-wk supplementation period, blood samples, aortic rings, and hearts were obtained for biochemical and physiological analyses. Feed or energy intakes did not differ among the 5 groups of rats. However, dietary supplementation with watermelon pomace juice or L-arginine increased serum concentrations of arginine; reduced fat accretion; lowered serum concentrations of glucose, free fatty acids, homocysteine, and dimethylarginines; enhanced GTP cyclohydrolase-I activity and tetrahydrobiopterin concentrations in the heart; and improved acetylcholine-induced vascular relaxation. Compared with the control, dietary supplementation with lycopene or citrus pectin did not affect any measured parameter. These results provide the first evidence to our knowledge for a beneficial effect of watermelon pomace juice as a functional food for increasing arginine availability, reducing serum concentrations of cardiovascular risk factors, improving glycemic control, and ameliorating vascular dysfunction in obese animals with type-II diabetes.
 ...
PMID:Dietary supplementation with watermelon pomace juice enhances arginine availability and ameliorates the metabolic syndrome in Zucker diabetic fatty rats. 1802 83


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>