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)

The role of dietary protein in weight loss and weight maintenance encompasses influences on crucial targets for body weight regulation, namely satiety, thermogenesis, energy efficiency, and body composition. Protein-induced satiety may be mainly due to oxidation of amino acids fed in excess, especially in diets with "incomplete" proteins. Protein-induced energy expenditure may be due to protein and urea synthesis and to gluconeogenesis; "complete" proteins having all essential amino acids show larger increases in energy expenditure than do lower-quality proteins. With respect to adverse effects, no protein-induced effects are observed on net bone balance or on calcium balance in young adults and elderly persons. Dietary protein even increases bone mineral mass and reduces incidence of osteoporotic fracture. During weight loss, nitrogen intake positively affects calcium balance and consequent preservation of bone mineral content. Sulphur-containing amino acids cause a blood pressure-raising effect by loss of nephron mass. Subjects with obesity, metabolic syndrome, and type 2 diabetes are particularly susceptible groups. This review provides an overview of how sustaining absolute protein intake affects metabolic targets for weight loss and weight maintenance during negative energy balance, i.e., sustaining satiety and energy expenditure and sparing fat-free mass, resulting in energy inefficiency. However, the long-term relationship between net protein synthesis and sparing fat-free mass remains to be elucidated.
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PMID:Dietary protein, weight loss, and weight maintenance. 1940 Jul 50

Diabetic nephropathy is the leading cause of renal failure in the United States. The obese Zucker rat (OZR; fa/fa) is a commonly used model of type 2 diabetes and metabolic syndrome (MetS), and of the nephropathy and renal oxidative stress commonly seen in these disorders. Heterozygous lean Zucker rats (LZRs; fa/+) are susceptible to high-fat diet (HFD)-induced obesity and MetS. The present study was designed to investigate whether 4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl (TEMPOL), a membrane-permeable radical scavenger, could alleviate the renal effects of MetS in OZR and LZR fed a HFD, which resembles the typical "Western" diet. OZR and LZR were fed a HFD (OZR-HFD and LZR-HFD) or regular diet (OZR-RD and LZR-RD) and allowed free access to drinking water or water containing 1 mmol/l TEMPOL for 10 weeks. When compared to OZR-RD animals, OZR-HFD animals exhibited significantly higher levels of total renal cortical reactive oxygen species (ROS) production, plasma lipids, insulin, C-reactive protein, blood urea nitrogen (BUN), creatinine (Cr), and urinary albumin excretion (P < 0.05); these changes were accompanied by a significant decrease in plasma high-density lipoprotein levels (P < 0.05). The mRNA expression levels of desmin, tumor necrosis factor-alpha (TNF-alpha), nuclear factor kappaB (NFkappaB), and NAD(P)H oxidase-1 (NOX-1) were significantly higher in the renal cortical tissues of OZR-HFD animals; NFkappaB p65 DNA binding activity as determined by electrophoretic mobility shift assay was also significantly higher in these animals. The same trends were noted in LZR-HFD animals. Our data demonstrate that TEMPOL may prove beneficial in treating the early stages of the nephropathy often associated with MetS.
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PMID:Diet-induced renal changes in Zucker rats are ameliorated by the superoxide dismutase mimetic TEMPOL. 1942 63

Diet and nutrition have played an important role in maintaining physiological homeostasis. Recent literature emphasizes potential therapeutic effects of micronutrients found in natural products, indicating positive applications for controlling the pathogenesis of chronic diseases driven by an inflammatory nidus. Nutritional compounds which display anti-inflammatory and antioxidant effects have specific applications in preventing oxidative stress induced injury which characterizes their pathogenesis. Patient control over diet and disease has been demonstrated in diabetes mellitus, cardiovascular disease, rheumatology, carcinogenesis and other diseases. Polyphenolic compounds are ubiquitous dietary components, mainly flavonoids and tannins. Specific polyphenols are effective in scavenging reactive oxygen and reactive nitrogen species. They are able to modulate genes associated with metabolism, stress defence, drug metabolizing enzymes, detoxification and transporter proteins. Their overall effect is protective in overcoming damaging effects of chronic diseases and in delaying the degenerative effects of ageing. The mechanisms involved in radical scavenging activity are complex, determined by the structure of the compound, redox status of the environment and interactions with other agents. Atherogenic dyslipidaemia associated with a pro-inflammatory pro-thrombotic state in metabolic syndrome and related risk of fatty liver, arthritis, neurodegenerative disorders and certain types of cancers are ideal therapeutic targets for bioactive phytochemicals which can combat oxidative stress induced damage at a sub-cellular level. It is relevant that purified micronutrients isolated from natural products may be less effective than a combination seen in the natural product due to synergistic effects of interacting agents. Some of these mechanisms and potential therapeutic targets are discussed.
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PMID:Relevance of nutritional antioxidants in metabolic syndrome, ageing and cancer: potential for therapeutic targeting. 1968 82

To compare the molecular composition and functional differences at the lipoprotein level, we analyzed individual lipoprotein fractions from male patients with metabolic syndrome (MetS) (n=10) and gender- and age-matched healthy controls (n=14). The MetS group had significantly higher obesity, blood pressure, serum cholesterol, triglyceride (TG), adiponectin, and uric acid levels than the control group, while the serum blood urea nitrogen and creatinine levels of the MetS group were in the normal range. The MetS group had much weaker serum antioxidant ability and were more susceptible to copper-mediated low-density lipoprotein (LDL)-oxidation. TG and apoC-III co-accumulated with LDL, high density lipoprotein (HDL)2, and HDL3 in the MetS group. The MetS group had serum amyloid A (SAA)-enriched HDL2 and HDL3, although the serum level of SAA was not higher than in controls. The MetS group had significantly deprived paraoxonase (PON) activity in the serum and HDL, while the MetS group had 38% higher serum cholesteryl ester transfer protein (CETP) activity than that of the control group. Many serum parameters, such as TG, apoC-III, and uric acid, were elevated in the MetS group, and most of these measures were enriched in the LDL and HDL fractions rather than the very low density lipoprotein (VLDL) fraction. The lipid and apolipoprotein composition of HDL was severely altered and its beneficial functions were severely diminished. ApoA-I level was more readily detected in lipoprotein-deficient serum of the MetS group, indicating that the apoA-I exists in a lipid-free state. These results suggest that the MetS group had dysfunctional HDL that enriched TG, apoC-III, CETP, and SAA without antioxidant activity.
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PMID:The functional and compositional properties of lipoproteins are altered in patients with metabolic syndrome with increased cholesteryl ester transfer protein activity. 1995 11

The objectives were to describe the association between body mass index (BMI, kg/m(2)), body composition and risk factors to metabolic diseases; observe the prevalence of metabolic syndrome and list the characteristics of overweight and obese women. Voluntaries (n=50; BMI=31+/-6; age=36+/-11 years old), were evaluated regarding clinical examination, anthropometrics measurements, samples of blood and urine, resting energy expenditure and food register. Phases in which they become obese in descending order: adulthood, pregnancy, adolescence, over 40 years old and after marriage. The odds to have one or more obese family members were 316%. They were anxious (60%), depressives (12%), compulsives (34%) and had sleep disturbance (32%). The odds to dyslipidemia was 28%, to hypertension was 25% and to glucose over 100 mg/dL 35%. They were in caloric deficit, but, nitrogen balance was positive. The metabolic syndrome was present in 25% of these women and was positively correlated with body fat indicators and age. The obesity of these women seems to be multifactorial with a family influence that could be caused by genetics and environment contributions. The emotional/physical balance should be influenced on this process.
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PMID:[Lifestyle and risk factors associated to body fat increase in women]. 2016 40

Recently it has been reported that low serum IL-10 levels are associated with an increased susceptibility for metabolic syndrome and type 2 diabetes mellitus (T2DM). We investigated whether the -1087G/A (rs1800896), -824C/T (rs1800871), -597C/A (rs1800872) IL-10 polymorphisms were associated with type 2 diabetes in a study on a cohort of Italian Caucasians comprising 490 type 2 diabetic and 349 control subjects. Stratifying the data according to IL-10 genotypes, trends for the progressive increase of glucose and neutrophil levels were observed in -1087GG vs. -1087GA vs. -1087AA positive diabetic patients (-1087GG<-1087GA<-1087AA). In addition, evaluating the laboratory parameters according to the -597/-824/-1087 derived haplotypes a significant increase of neutrophils was found in diabetic vs. non-diabetic -597A/ -824T/-1087A positive subjects (Student t test = 3.707, p<0.01). In an attempt to integrate clinical laboratory and immunogenetic data to determine whether these factors taken together define sufficient risk sets for type 2 diabetes we performed the grade-of-membership analysis (GoM). GoM allowed to identify a population of subjects negative for IL-10 -824T allele, 74.4% of which were diabetic patients characterised by vascular damages (Chronic kidney failure and/or Myocardial Infarction), reduction of haematocrit, increase of blood urea nitrogen, creatinin and monocyte levels. These data seem to suggest that -597A/-824T/-1087A negative subjects are more prone to the major type 2 diabetic vascular damages and allow to hypothesise that the contemporary evaluation of some simple hematochemical parameters and IL-10 SNPs may allow identifying diabetic patients with the worse prognostic profile, needing both better complication prevention planning and therapeutic strategies.
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PMID:Risk profiles in type 2 diabetes (metabolic syndrome): integration of IL-10 polymorphisms and laboratory parameters to identify vascular damages related complications. 2038 4

Few cases of nephrolithiasis (renal calculi) have been reported in bottlenose dolphins Tursiops truncatus. A case-control study was conducted to compare ultrasonographic images and clinicopathologic serum and urine values among 14 dolphins with nephrolithiasis (mild cases: 1 to 19 nephroliths, n = 8; advanced cases: > or = 20 nephroliths, n = 6) to 6 controls over an 18 mo period. Archived nephroliths collected postmortem from 7 additional bottlenose dolphins were characterized using quantitative analysis. All advanced cases had bilateral nephroliths, and 67% had visible collecting ducts. During the study, 2 of the advanced cases developed hydronephrosis, and 1 of these cases had ureteral obstruction due to a nephrolith. Compared to controls, cases (mild and advanced) were significantly more likely to have anemia (hematocrit [HCT] < 38%), high blood urea nitrogen (>59 mg dl(-1)), high creatinine (>1.9 mg dl(-1)), and low estimated glomerular filtration rate (<150 ml min(-1) 2.78 m(-2)). Advanced-case urine samples were more likely to have erythrocytes, occult blood, and lower pH compared to mild cases and controls. Mean serum uric acid among all study groups was low (0.15 to 0.27 mg dl(-1)). Urinary uric acid concentrations were highest among mild cases (272 mg g(-1) creatinine), but advanced cases had levels lower than that of controls (40 and 127 mg g(-1) creatinine, respectively). All nephroliths were characterized as 100% ammonium acid urate. We conclude that nephrolithiasis is clinically relevant in dolphins and can decrease renal function and HCT. The presence of nephrolithiasis, presumably ammonium acid urate nephrolithiasis, in the face of low serum uric and relatively low urinary uric acid in advanced cases may indicate a metabolic syndrome similar to that reported in humans.
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PMID:Clinical relevance of urate nephrolithiasis in bottlenose dolphins Tursiops truncatus. 2040 34

Oxidative stress plays a key role in the pathophysiology of coronary artery disease, and constitutes a common mechanism behind the risk factors associated with this disease such as atherosclerosis, hypertension, diabetes and the metabolic syndrome. Oxidative stress is defined as an imbalance between the production of reactive oxygen and nitrogen species and the detoxification by the appropriate cellular systems. Reactive oxygen species induce cardiovascular dysfunction by modulating cell contraction/dilation, migration, growth/apoptosis and extracellular matrix protein turnover, which contribute to vascular and cardiac remodeling. In the last decade, the NADPH oxidase family has emerged as one of the most relevant sources of reactive oxygen species within the cardiovascular system. Recent data suggest a significant role of the genetic background in NADPH oxidase regulation. Common genetic polymorphisms within the promoter and exonic sequences of CYBA, the gene that encodes the p22phox subunit of the NADPH oxidase, have been characterized in the context of cardiovascular diseases. This review aims to present the current state of research into these polymorphisms with regards to their relationship to coronary artery disease.
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PMID:CYBA gene variants as biomarkers for coronary artery disease. 2060 55

The metabolic syndrome is a clustering of risk factors of metabolic origin that increase the risk for cardiovascular disease and type 2 diabetes. A proposed central event in metabolic syndrome is a decrease in the amount of bioavailable nitric oxide (NO) from endothelial NO synthase (eNOS). Recently, an alternative pathway for NO formation in mammals was described where inorganic nitrate, a supposedly inert NO oxidation product and unwanted dietary constituent, is serially reduced to nitrite and then NO and other bioactive nitrogen oxides. Here we show that several features of metabolic syndrome that develop in eNOS-deficient mice can be reversed by dietary supplementation with sodium nitrate, in amounts similar to those derived from eNOS under normal conditions. In humans, this dose corresponds to a rich intake of vegetables, the dominant dietary nitrate source. Nitrate administration increased tissue and plasma levels of bioactive nitrogen oxides. Moreover, chronic nitrate treatment reduced visceral fat accumulation and circulating levels of triglycerides and reversed the prediabetic phenotype in these animals. In rats, chronic nitrate treatment reduced blood pressure and this effect was also present during NOS inhibition. Our results show that dietary nitrate fuels a nitrate-nitrite-NO pathway that can partly compensate for disturbances in endogenous NO generation from eNOS. These findings may have implications for novel nutrition-based preventive and therapeutic strategies against cardiovascular disease and type 2 diabetes.
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PMID:Dietary inorganic nitrate reverses features of metabolic syndrome in endothelial nitric oxide synthase-deficient mice. 2087 22

An abnormal production of reactive oxygen species (ROS) and the subsequent decrease in vascular bioavailability of nitric oxide (NO) have long been proposed to be the common pathogenetic mechanism of the endothelial dysfunction, resulting from diverse cardiovascular risk factors such as hypercholesterolaemia, diabetes mellitus, chronic smoking, metabolic syndrome, and hypertension. Superoxide produced by the nicotinamide dinucleotide phosphate (NADPH) oxidase, mitochondrial sources, or the xanthine oxidase may react with NO, thereby resulting in excessive formation of peroxynitrite, a reactive nitrogen species that has been demonstrated to accelerate the atherosclerotic process by causing direct structural damage and by causing further ROS production. Despite this sound biological rationale and a number of pre-clinical and clinical lines of evidence, studies testing the effects of classical antioxidants such as vitamin C, vitamin E, or folic acid in combination with vitamin E have been disappointing. Rather, substances such as statins, angiotensin-converting enzyme inhibitors, or AT1-receptor blockers, which possess indirect antioxidant properties mediated by the stimulation of NO production and simultaneous inhibition of superoxide production (e.g. from the NADPH oxidase), have been shown to improve vascular function in pre-clinical and clinical studies and to reduce the incidence of cardiovascular events in patients with cardiovascular disease. Today, oxidative stress remains an attractive target for cardiovascular prevention and therapy. However, a deeper understanding of its source, and of its role in vascular pathology, is necessary before new trials are attempted.
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PMID:Is oxidative stress a therapeutic target in cardiovascular disease? 2097 1


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