Sonneratia apetala seed oil attenuates potassium oxonate/hypoxanthine-induced hyperuricemia and renal injury in mice.

Sonneratia apetala seeds are considered as prospective nutraceuticals with a high content of unsaturated fatty acids (UFAs) which are mainly distributed in the oil. It is well-known that UFAs could exhibit urate-lowering potency and protect against renal injury, indicating that S. apetala seed oil (SSO) may possess hypouricemic and nephroprotective effects. Consequently, the present work attempted to probe into the effects and mechanisms of SSO on potassium oxonate/hypoxanthine-induced hyperuricemia and associated renal injury. The results indicated that SSO treatment prominently inhibited the increase of serum uric acid (UA), creatinine (CRE), and urea nitrogen (BUN) levels and hepatic xanthine oxidase (XOD) activity in hyperuricemia mice. Kidney indexes and histopathological lesions were also remarkably ameliorated. Additionally, SSO treatment improved the renal anti-oxidant status in hyperuricemia mice by significantly reversing the increase in ROS and MDA levels as well as the decline in SOD, CAT and GSH-Px activities. SSO dramatically downregulated the expression and secretion of pro-inflammatory factors involving MCP-1, IL-1ß, IL-6, IL-18 and TNF-α elicited by hyperuricemia. Furthermore, after SSO treatment, increased protein expressions of GLUT9, URAT1 and OAT1 in the hyperuricemia mice were obviously reversed. SSO treatment enormously restored Nrf2 activation and subsequent translation of related anti-oxidative enzymes in the kidneys. TXNIP/NLRP3 inflammasome activation was also obviously suppressed by SSO. In conclusion, SSO exerted favorable hypouricemic effects owing to its dual functions of downregulating the XOD activity and modulating the expressions of renal urate transport-associated proteins, and it also could alleviate hyperuricemia-induced renal injury by restoring the Keap1-Nrf2 pathway and blocking the TXNIP/NLRP3 inflammasome activation.

Limosilactobacillus fermentum JL-3 isolated from "Jiangshui" ameliorates hyperuricemia by degrading uric acid.

Recent studies into the beneficial effects of fermented foods have shown that this class of foods are effective in managing hyperuricemia and gout. In this study, the uric acid (UA) degradation ability of Limosilactobacillus fermentum JL-3 strain, isolated from "Jiangshui" (a fermented Chinese food), was investigated. In vitro results showed that JL-3 strain exhibited high degradation capacity and selectivity toward UA. After oral administration to mice for 15 days, JL-3 colonization was continuously detected in the feces of mice. The UA level in urine of mice fed with JL-3 was similar with the control group mice. And the serum UA level of the former was significantly lower (31.3%) than in the control, further confirmed the UA-lowering effect of JL-3 strain. Limosilactobacillus fermentum JL-3 strain also restored some of the inflammatory markers and oxidative stress indicators (IL-1ß, MDA, CRE, blood urea nitrogen) related to hyperuricemia, while the gut microbial diversity results showed that JL-3 could regulate gut microbiota dysbiosis caused by hyperuricemia. Therefore, the probiotic Limosilactobacillus fermentum JL-3 strain is effective in lowering UA levels in mice and could be used as a therapeutic adjunct agent in treating hyperuricemia.

Anti-hyperuricemic and nephroprotective effects of whey protein hydrolysate in potassium oxonate induced hyperuricemic rats.

BACKGROUND: Hyperuricemia (HUA) is a serious public health concern globally that needs to be solved. It is closely related to gout and other metabolic diseases. To develop a safe and effective dietary supplementation for alleviating HUA, we investigated the effects of whey protein hydrolysate (WPH) on HUA and associated renal dysfunction and explored their underlying mechanism. RESULTS: Potassium oxonate was used to induce HUA in model rats, who were then administered WPH for 21 days. The results showed that WPH significantly inhibited xanthine oxidase and adenosine deaminase activity in serum and liver, decreased uric acid (UA), creatinine, and blood urea nitrogen levels in serum, and increased the UA excretion in urine. In addition, WPH downregulated the expression of urate transporter 1 and upregulated the expression of organic anion transporter 1, adenosine triphosphate binding cassette subfamily G member 2, organic cation/carnitine transporters 1 and 2, and organic cation transporter 1 in kidneys. CONCLUSION: These findings demonstrated for the first time that WPH could alleviate HUA by inhibiting UA production and promoting UA excretion, and improve the renal dysfunction caused by HUA. Thus, WPH may be a potential functional ingredient for the prevention and treatment of HUA and associated renal dysfunction. © 2021 Society of Chemical Industry.

Determination of total purine and purine base content of 80 food products to aid nutritional therapy for gout and hyperuricemia.

The aim of this work is to facilitate the nutritional therapy of gout and hyperuricemia. In Japan, patients with gout or hyperuricemia are recommended to consume less than 400 mg of dietary purines per day. When receiving nutritional therapy for gout or hyperuricemia, purine-rich foods (>200 mg/100 g) should be eaten in even lower quantities. The purine content of foods reported in this study are as follows: noodles, 0.6-12.1 mg/100 g; bread, 4.4 mg/100 g; peas or seeds, 19.6-67.1 mg/100 g; dairy, 0.0-1.4 mg/100 g; Japanese vegetables, 0.9-47.1 mg/100 g; seasonings, 0.7-847.1 mg/100 g; meat or fish, 19.0-385.4 mg/100 g; fish milt, 375.4-559.8 mg/100 g; and supplements, 81.9-516.0 mg/100 g. Foods containing very large amounts of purine (>300 mg/100 g) included anchovy, cutlassfish (hairtail), cod milt, globefish milt, dried Chinese soup stock, dried yeast, a Euglena supplement, and a Lactobacillus supplement. When eating these high-purine food or supplements, the quantity taken at one meal should be limited, especially milt because they typically consumed amount of 20-30 g is equivalent to 75-168 mg total purines. This is 20%-40% of the recommended daily amount (400 mg/day) for patients with gout or hyperuricemia. Thus, these patients should restrict the amount of purine-rich foods they consume. Good dietary habits with a good balance of nutrients are recommended.

Comparisons of protective effects between two sea cucumber hydrolysates against diet induced hyperuricemia and renal inflammation in mice.

Hyperuricemia is an important risk factor for many diseases including hypertension and type 2 diabetes. This study investigated and compared the effects of hydrolysates of two sea cucumber species, Apostichopus japonicus and Acaudina leucoprocta, on the alleviation of diet-induced hyperuricemia and renal inflammation. The structure and abundance of oligopeptides in enzymatic hydrolysates of A. japonicus (EH-JAP) and A. leucoprocta (EH-LEU) were identified via MALDI-TOF/TOF-MS, and the anti-hyperuricemic and anti-inflammatory effects of the hydrolysates were explored in a diet-induced hyperuricemic mouse model. Both EH-JAP and EH-LEU inhibit uric acid biosynthesis and promote uric acid excretion, leading to the alleviation of the hyperuricemic phenotype. In addition, these two treatments down-regulated the transcription of pro-inflammatory cytokines, up-regulated the transcription of anti-inflammatory cytokines, and inhibited the activation of the Toll-like receptor 4/myeloid differentiation factor 88/NF-kappaB (TLR4/MyD88/NF-κB) signaling pathway, leading to the alleviation of renal inflammation. EH-JAP had better effects than EH-LEU due to differences in their regulation of uric acid biosynthesis, uric acid excretion and release of anti-inflammatory cytokines. In addition, EH-JAP and EH-LEU treatment alleviated the dysfunction of the gut microbiota by increasing the abundance of beneficial Lactobacillus and short-chain fatty acid producers and decreasing the abundance of opportunistic pathogens. This study provides a valuable reference for the development of sea cucumber applications.

[Efficiency estimation of diet therapy with protein component modification in patients with obesity and purine metabolism disorder].

The development of a personalized nutritional approach to diet therapy for patients with obesity and hyperuricemia, aimed at increasing the treatment effectiveness of these patients, is an urgent task. The aim: to assess the impact of nutritional approach with a modification of the protein component on body composition and biochemical parameters in patients with obesity and purine metabolism disorder. Material and methods. A randomized controlled trial was conducted, and included 50 patients (average age 46.9±2.5 years) with obesity and purine metabolism disorder. All patients were divided into two groups of 25 people. Within 2 weeks patients of group 1 received the main version of a standard low-calorie diet (1730 kcal, protein - 87.4 g, fat - 61.4 g, carbohydrates - 207 g). Group 2 received a personalized version of the diet (2125 kcal, protein - 100.2 g, fat - 75.9 g, carbohydrate - 260 g) with the modification of the protein component: protein content of at least 90 g per day, restriction of animal products containing a high purine load. Results and discussion. During diet therapy the decrease in fat mass in group 1 patients averaged 4.4%, visceral fat area - 8.6% (p<0.05) and in patients of group 2 - 6.9 and 9.1% respectively (p<0.05). During treatment a significant decrease in muscle mass was observed in group 1 at average 3.9% (p<0.05), and in group 2 on the basis of personal nutritional approach there was a slight decrease in muscle mass at average of 1.5%. After treatment patients of the two groups showed improvement in a number of indicators of lipid and carbohydrate metabolism: a significant decrease (p<0.05) of glucose, total cholesterol, LDL cholesterol and triglycerides in blood serum by 18.2-19.1, 23.2-23.6, 24.2-25.0 и 28.5-30.4%. However, patients in group 1 showed a slight decrease in uric acid in blood serum at average 7.6%, and patients in group 2 who received a personal nutritional approach with a modification of the protein component showed a significant decrease in uric acid at average of 12.5% (p<0.05). Conclusion. The obtained data indicate the need for a personal nutritional approach with a modification of the protein component in patients with obesity and purine metabolism disorder, which will prevent the development and progression of complications associated with obesity.

Dietary Interventions for Gout and Effect on Cardiovascular Risk Factors: A Systematic Review.

Gout is one of the most prevalent inflammatory rheumatic disease. It is preceded by hyperuricemia and associated with an increased risk for cardiovascular disease, both related to unhealthy diets. The objective of this systematic review is to better define the most appropriate diet addressing both disease activity and traditional cardiovascular risk factors in hyperuricemic patients. We included clinical trials with patients diagnosed with hyperuricemia or gout, investigating the effect of dietary interventions on serum uric acid (SUA) levels, gout flares and-if available-cardiovascular risk factors. Eighteen articles were included, which were too heterogeneous to perform a meta-analysis. Overall, the risk of bias of the studies was moderate to high. We distinguished four groups of dietary interventions: Calorie restriction and fasting, purine-low diets, Mediterranean-style diets, and supplements. Overall, fasting resulted in an increase of SUA, whilst small (SUA change +0.3 to -2.9 mg/dL) but significant effects were found after low-calorie, purine-low, and Mediterranean-style diets. Studies investigating the effect on cardiovascular risk factors were limited and inconclusive. Since Mediterranean-style diets/DASH (Dietary Approach to Stop Hypertension) have shown to be effective for the reduction of cardiovascular risk factors in other at-risk populations, we recommend further investigation of such diets for the treatment of gout.

Dietary Antioxidant Supplements and Uric Acid in Chronic Kidney Disease: A Review.

Increased serum levels of uric acid have been associated with the onset and development of chronic kidney disease (CKD), cardiovascular disease, and mortality, through several molecular pathogenetic mechanisms, such as inflammation and oxidative stress. Oxidative stress is present even in the early stages of CKD, progresses parallelly with the deterioration of kidney function, and is even more exacerbated in end-stage renal disease patients undergoing maintenance hemodialysis. Although acting in the plasma as an antioxidant, once uric acid enters the intracellular environment; it behaves as a powerful pro-oxidant. Exogenous intake of antioxidants has been repeatedly shown to prevent inflammation, atherosclerosis and oxidative stress in CKD patients. Moreover, certain antioxidants have been proposed to exert uric acid-lowering properties. This review aims to present the available data regarding the effects of antioxidant supplements on both oxidative stress and uric acid serum levels, in a population particularly susceptible to oxidative damage such as CKD patients.

Male asymptomatic hyperuricemia patients display a lower number of NKG2D+ NK cells before and after a low-purine diet.

BACKGROUND: Aberrant activation of the immune system has been reported in asymptomatic hyperuricemia (HUA) patients. However, very few studies have elucidated the role of natural killer (NK) cells in this disease. METHODS: In this study, we evaluated the relationship between NK cells and HUA in 16 control subjects and 20 patients, who were all on a low-purine diet. We analyzed the number of circulating NK cells, its subsets, interferon-γ, and CD107 NK cells, by flow cytometry, before and after 4 and 24 weeks of diet control. We also assessed the potential association of the NK cells with clinical measures. RESULTS: The patients consistently had a lower number of NKG2D NK cells before and after low-purine diet, even the serum uric acid (SUA) levels <7 mg/dL after diet control. Moreover, a lower number of NK cells and a higher number of CD107a NK cells were observed on recruitment. Low-purine diet was benefit on the improvement of the SUA levels, body mass index (BMI), and the number and functions of NK cells. Furthermore, the number of CD3CD56 NK cells and NKG2D NK cells negatively correlated with the BMI before and after diet control. CONCLUSION: The consistent lower number of NKG2D NK cells and correlated with BMI before and after low-purine diet may be involved in the occurrence and development of HUA.

Uric Acid: The Unknown Uremic Toxin.

This review brings together concepts of uric acid metabolism affecting renal parenchyma and its function and the current therapies to reduce hyperuricemia (HyU) and avoid renal disease progression. High uric acid plays an important role in several chronic diseases including kidney diseases such as lithiasis, gout nephropathy, and preeclampsia. In the last 30 years, it has been shown that reducing HyU with low protein and low purine diets in addition to allopurinol creates physiopathological conditions that produce a slight increase in the glomerular filtration rate (GFR). In recent years, in a new era of research in clinical, genetics, pharmacological, and epidemiologic fields, they have been moving forward to support the idea that reduction in HyU could benefit the chronic renal failure (CRF) patients (stage III-IV), thereby avoiding the drop of GFR for undefined mechanisms. There are several clinical trials in progress that show the HyU reducing to very low values and an increased GFR. In a young population, when treating HyU there is a reduction in high blood pressure. There are some reports showing that HyU could play a role in the diabetic nephropathy. Therefore, there have been some speculations that HyU treatment could stop the progression of CRF modifying the natural history of the diseases. So there will be new clinical trials with old and new medication and metabolic procedure to maintain a very low blood levels in the unknown uremic toxin know as uric acid which seems to be the toxin to the damage kidney.

Moderation of hyperuricemia in rats via consuming walnut protein hydrolysate diet and identification of new antihyperuricemic peptides.

In this study, walnut meal hydrolysates (WMH) and dephenolized walnut meal hydrolysates (DWMH) were found to effectively decrease the serum uric acid level and protect the renal function in potassium oxonate-induced hyperuricemic rats in vivo as well as inhibit xanthine oxidase in vitro. Two novel antihyperuricemic peptides including WPPKN (640.8 Da) and ADIYTE (710.7 Da) were purified from DWMH via Sephadex G-15 gel filtration and reverse-phase high-performance liquid chromatography and identified by LC-ESI-MS/MS. These peptides displayed high in vitro xanthine oxidase inhibition (XOI) activity with IC50 values of 17.75 ± 0.12 mg mL-1 (WPPKN) and 19.01 ± 0.23 mg mL-1 (ADIYTE). Based on the results of molecular simulation, WPPKN entered into the hydrophobic channel and even obstructed the interaction between xanthine and xanthine oxidase (XO), while ADIYTE was positioned on the surface of the B-chain and blocked the entrance of the substrate to the hydrophobic channel. Therefore, the two peptides are partially responsible for the antihyperuricemic properties of DWMH.

Nutrición e hiperuricemia / Nutrition and hyperuricemia

El aumento de la incidencia y prevalencia de hiperuricemia asintomática, la que está fuertemente asociada a los factores de riesgo cardiovasculares clásicos y la dificultad para definir su tratamiento con drogas ha jerarquizado al tratamiento dietético, a los efectos de identificar los alimentos que pueden tener efectos protectores sobre el nivel de ácido úrico plasmático (AU). Los niveles del AU dependen de la producción endógena (10%), disminución de la excreción (90%) o de ambas. La producción del AU depende de la ingesta de purina, sin embargo, una dieta rica en purina sería responsable solo de un aumento en 1 a 2 mg / dl del AU sérico. La pérdida < 5 kg disminuye hasta un 45% el riesgo de aumentar el AU, mientras que pérdidas superiores reducirían al menos el 60% del riesgo. De igual manera, el descenso del peso máximo y la estabilidad del peso disminuyen el riesgo de hiperuricemia. Se sugiere que este descenso no sea brusco para evitar el catabolismo muscular que puede conducir a sarcopenia con pérdida de la fuerza y debilidad muscular y aumento concomitante del AU. Reducen los niveles séricos de AU: leche, yogur y quesos blancos, las frutas ricas en vitamina C, huevos, frutas secas sin sal, legumbres (incluidas la soja) y pollo, salmón, bacalao y langosta. Debe limitarse las carnes rojas (cerdo, ternera, cabrito), y evitarse mariscos, pescados (trucha, atún, palometa, vieir

The increase of incidence and prevalence of asymptomatic hyperuricemia, closely related to the traditional cardiovascular risk factors, and the difficulty to establish a drug therapy for this condition have attached importance to dietary treatment; the aim is to identify foods which can prevent plasma uric acid (UA) concentrations from reaching abnormally high levels. UA level depends on endogenous production (10%), reduced excretion (90%) or both. Although UA production depends on the consumption of purine, a diet rich in purines is believed to be responsible only for a serum UA increase of 1 to 2 mg/dL. Losing < 5 kg reduces the risk of UA increase by up to 45%, whereas higher losses could lead to a risk at least 60% lower. In the same way, maximum weight loss and weight stability minimize the risk of hyperuricemia. Weight loss, however, should not be sudden so as to avoid muscle catabolism, which may cause loss of muscle mass and strength (sarcopenia) and a concomitant UA increase. The following foods can help reduce serum UA levels: milk, yogurt, fresh cheese, vitamin C-rich fruits, eggs, unsalted nuts, legumes (including soy), chicken, salmon, codfish and lobster. Red meat intake (pork, beef, goat meat) should be limited, and seafood, fish (trout, tuna, pompano, scallop, anchovy, herring, sardine and tuna in oil), bacon, viscera, turkey and lamb should be avoided.

Update on Importance of Diet in Gout.

Gout is an inflammatory arthritis caused by deposition of monosodium urate crystals within synovial joints. Although it is most well-known for its arthritis, gout has an intimate relationship with many other cardiovascular and metabolic conditions. Current recommendations support aggressive medical therapy to treat gout, whereas dietary counseling has become less emphasized. This article argues for the absolute importance of dietary counseling in gout and proves why this counseling may impact the long term well-being of a patient with gout.

Effect of Soy Sauce on Serum Uric Acid Levels in Hyperuricemic Rats and Identification of Flazin as a Potent Xanthine Oxidase Inhibitor.

This is the first report on the ability of soy sauce to effectively reduce the serum uric acid levels and xanthine oxidase (XOD) activities of hyperuricemic rats. Soy sauce was partitioned sequentially into ethyl acetate and water fractions. The ethyl acetate fraction with strong XOD inhibition effect was purified further. On the basis of xanthine oxidase inhibitory (XOI) activity-guided purification, nine compounds including 3,4-dihydroxy ethyl cinnamate, diisobutyl terephthalate, harman, daidzein, flazin, catechol, thymine, genistein, and uracil were obtained. It was the first time that 3,4-dihydroxy ethyl cinnamate and diisobutyl terephthalate had been identified from soy sauce. Flazin with hydroxymethyl furan ketone group at C-1 and carboxyl at C-3 exhibited the strongest XOI activity (IC50 = 0.51 ± 0.05 mM). According to fluorescence quenching and molecular docking experiments, flazin could enter into the catalytic center of XOD to interact with Lys1045, Gln1194, and Arg912 mainly by hydrophobic forces and hydrogen bonds. Flazin, catechol, and genistein not only were potent XOD inhibitors but also held certain antioxidant activities. According to ADME (absorption, distribution, metabolism, and excretion) simulation in silico, flazin had good oral bioavailability in vivo.

Comparison of the effect of high fruit and soybean products diet and standard diet interventions on serum uric acid in asymptomatic hyperuricemia adults: an open randomized controlled trial.

The aim of this study was to compare the effect of high fruit and soybean products diet and standard diet interventions on serum uric acid (SUA) in asymptomatic hyperuricemia adults. A total of 187 Chinese adults (20-59 years old) with asymptomatic hyperuricemia participated in this randomized trial and were assigned to receive the standard diet recommended by guideline (group 1) and high fruit and soybean products diet (group 2) for 3 months. The outcome of SUA was assessed before and at the end of the intervention period. After 3 months, the SUA in group 1 and group 2 was significant reduced, whereas the SUA was not significantly changed in-between groups. These data suggest that over a 3-month period, although the high fruit and soybean products diet and standard diet interventions yield no different effects on SUA, the high fruit and soybean products dietary intervention could be an effective alternative to a standard diet for achieving clinically important reductions in SUA for asymptomatic hyperuricemia patients.

Cross-sectional analysis of nutrition and serum uric acid in two Caucasian cohorts: the AusDiab Study and the Tromsø study.

BACKGROUND: Hyperuricemia can lead to gout, and may be a risk factor for cardiovascular events, hypertension, diabetes and renal disease. There is well-known link between gout and habitual intake of meat and seafood, however the association between hyperuricemia and micro-and macro-nutrient intake has not been established. METHODS: We studied associations between intakes of food categories, macro-and micronutrients and serum uric acid (SUA) levels in two cross-sectional surveys of Caucasian adults deriving from different food traditions: Australian Diabetes, Obesity and Lifestyle Study 1999/00 (n=9734, age 25-91) and Tromsø Study 4 1994/95 (n = 3031, age 25-69). Dietary intake was calculated from self-administered Food Frequency Questionnaires. In some analyses we stratified according to abdominal obesity status and gender. RESULTS: In both cohorts, lower levels of SUA were found in subjects with higher consumption of carbohydrates, calcium and vitamin B2, while higher fat intake was associated with higher SUA, after adjustment for age, body mass index, estimated glomerular filtration rate, physical activity, total energy intake, use of diuretics, presence of hypertension, diabetes and gout. Among individual food items, high consumption of dairy products, high-fibre bread, cereals and fruits were associated with lower SUA in most subject groups while consumption of meat, eggs, beer and spirits, but not wine, with elevated levels. CONCLUSIONS: Healthy food choices with high intake of carbohydrates, dairy products, fiber and micronutrient-rich foods, and limited intake of fat, beer and spirits, might be recommended to prevent high SUA. Dietary factors seem to have qualitatively similar impact on SUA in obese and non-obese men and women from Australia and Norway.

Componentes clásicos y no tradicionales del síndrome metabólico en niños y adolescentes con exceso ponderal / Classic and nontraditional components of metabolic syndrome in overweight children and adolescents

Introducción: Los componentes del Síndrome Metabólico (SM) en niños son complicaciones que sin intervención oportuna tendrán repercusiones dramáticas, antes de llegar a la adultez. Objetivos: Identificar y comparar componentes clá- sicos y no tradicionales del síndrome metabólico en ni- ños y adolescentes con exceso ponderal. Material y métodos: Estudio transversal en pacientes 6-15 años con exceso ponderal. Variables: Circunferencia de cintura (cm), glucosa(mg/dl), lipoproteína de alta densidad (mg/dl), triglicéridos(mg/dl), presión arterial (mm/Hg), insulina(µU/ml), índice de resistencia insulínica (HOMA), acantosis nigricans (AN), ácido úrico (mg/dl) e hígado graso no alcohólico. Protocolo: estándares internacionales para edad y gé- nero de variables y ultrasonido hepático, diagnóstico de SM por Federación Internacional de Diabetes (FID) y Asociación Latinoamericana de Diabetes (ALAD). Estadística. Frecuencias, porcentajes y X2. Resultados: N= 172. 55.2% sexo femenino, 69.8% adolescentes (11-15 años), 30.2% niños en etapa escolar (6-10 años). Promedio de edad: 11.7 ± 2.3. Componentes de SM: Obesidad visceral 94%; pre-hipertensión 18%; hipertensión arterial 25.6%; hipertrigliceridemia 72.6%; HDL bajo 59.3%; Hiperglucemia 6.4%; Hiperuricemia 52.9%; Hiperinsulinemia 76.7%; Resistencia Insulínica (HOMA) 80.8%; Diabetes Mellitus 2.3%; AN 88.4% e Hígado graso no alcohólico 14%.Diagnóstico de SM: 48.8%. La hipertensión arterial, hiperinsulinemia, RI, hiperuricemia y AN fueron más frecuentes en adolescentes. Un componente fue mayor en niños (p 0.017) y 4 componentes en adolescentes (p 0.002). Conclusiones: Los componentes más frecuentes del SM en pediatría son factores de riesgo cardiovascular, la hiperuricemia es componente novel que debiera investigarse por ser predictor de daño endotelial. Los niños presentaron menos componentes, aumentando en cantidad y severidad en adolescentes (AU)

Introduction: The components of the metabolic syndrome (MS) in children are complications that without opportune intervention will cause dramatic repercussions before reaching adulthood. Aim: To Identify and compare the traditional and nontraditional components of the metabolic syndrome in overweight children and adolescents. Methods: A cross-sectional study was performed using data from 172 obese patients (6-15 years old). The variables analyzed were: Waist circumference (cm), glucose (mg / dl), high density lipoprotein (mg / dl), triglycerides (mg / dl), blood pressure (mm / Hg), insulin (microU / ml), index insulin resistance (HOMA), acanthosis nigricans (AN), uric acid (mg / dl) and NAFLD. Protocols: International standards for age and gender applied to the variables and liver ultrasound, diagnosis of MS by the International Diabetes Federation (IDF) and Latin American Diabetes Association (ALAD). The statistics performed were frequencies, percentages and X2. Results: N = 172. 55.2% female, 69.8% adolescents (11-15 years), 30.2% children (6-10 years). Average age: 11.7 ± 2.3. Components of MS: visceral obesity 94%; pre-hypertension 18%; hypertension 25.6%; hypertriglyceridemia 72.6%; Low HDL 59.3%; Hyperglycemia 6.4%; Hyperuricemia 52.9%; Hyperinsuli nemia 76.7%; Insulin Resistance (HOMA) 80.8%; Diabetes Mellitus 2.3%; AN 88.4% and Nonalcoholic fatty liver 14%. Diagnosis of MS: 48.8%. Hypertension, hyperinsulinemia, RI, hyperuricemia and AN were more common in adolescents. One component was higher in children (p 0.017) and 4 components in adolescents (p 0.002). Conclusions: The most frequent pediatric components of MS are cardiovascular risk factors, the hyperuricemia is a novel component that should be investigated for being predictor of endothelial damage. The children had fewer components, increasing in quantity and severity in adolescents (AU)

[The principles of nutrition therapy of gout and hyperuricemia]. / Zasady dietoterapil dny moczanowej i hiperurykemii.

In 2012 the updated guidelines for the treatment of gout were published by the American College of Rheumatology (ACR), which underline the necessity of comprehensive treatment in this condition. According to the European League Against Rheumatism (EULAR), treatment of comorbidities, lifestyle modifications and proper diet may be of significant importance. In the primary care settings in Poland there is virtually no access to qualified dieticians. The nutritional counseling is sometimes implemented--usually to a very limited extent--by primary care physicians. It is believed that proper diet may improve the prognosis and quality of life in patients with gout. The aim of the work is to present the principles of nutrition therapy in gout and hyperuricemia, in the context of their pathogenesis. The key principles of nutrition therapy in the above mentioned conditions include a restriction of purine amount in the diet and reaching the proper body weight. Optimal hydration and alcohol elimination are also beneficial. Furthermore, some food ingredients can affect the plasma level of uric acid in the mechanisms irrelevant of their purine load.

Short communication: Effect of commercial or depurinized milk diet on plasma advanced oxidation protein products, cardiovascular markers, and bone marrow CD34+ stem cell potential in rat experimental hyperuricemia.

Cardiovascular repair and myocardial contractility may be improved by migration of bone marrow stem cells (BMSC) and their delivery to the site of injury, a process known as BMSC homing. The aim of our study was to examine the dietary effect of a newly patented depurinized milk (DP) that is almost free of uric acid and purine and pyrimidine compounds compared with a standard commercial 1.5% fat UHT milk diet or allopurinol therapy in rat experimental hyperuricemia. Bone marrow stem cell potential (BMCD34(+), CD34-postive bone marrow cells), plasma oxidative stress parameters [advanced oxidation protein products, AOPP) and thiobarbituric acid reactive substances (TBARS)], myocardial damage markers [creatine phosphokinase (CPK), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH)], plasma cholesterol, and high-density lipoprotein cholesterol were investigated. The DP milk diet significantly increased the number of BMCD34(+) stem cells compared with commercial UHT milk. Allopurinol given alone also increased the number of BMCD34(+). Hyperuricemia caused a significant increase in all plasma enzyme markers for myocardial damage (CPK, LDH, and AST). A cardioprotective effect was achieved with allopurinol but almost equally with DP milk and more than with commercial milk. Regarding plasma AOPP, TBARS, and cholesterol levels, the most effective treatment was DP milk. In conclusion, the protective role of a milk diet on cardiovascular function may be enhanced through the new depurinized milk diet, which may improve cardiovascular system function via increased bone marrow stem cell regenerative potential, decreased plasma oxidative stress parameters, and decreased levels of myocardial damage markers and cholesterol. New dairy technology strategies focused on eliminating harmful milk compounds should be completely nontoxic. Novel milk products should be tested for their ability to improve tissue repair and function.