Search

Objective: Hyperuricemia, which occurs as a result of high uric acid levels, the end product of purine metabolism, is related with asymptomatic hyperuricemia (ASH) when it does not show symptoms and gouty arthritis (GOUT) when urate crystals occur. Hyperuricemia may interact with metabolic syndrome components. Therefore, the aim of the study was to assess the relationship of GOUT and ASH with metabolic syndrome. Methods: The study was conducted with 145 individuals diagnosed with GOUT and ASH. Data on general characteristics, biochemical test results (serum fasting insulin, fasting blood glucose, uric acid, and blood lipids (such as low-density lipoprotein, total cholesterol, triglyceride, and high-density lipoprotein)), anthropometric (waist and hip circumferences, body weight and height) and blood pressure (systolic and diastolic) measurement results were collected. Bioelectrical Impedance Analysis was used to measure body composition. The National Cholesterol Education Program-Adult Treatment Panel III (NCEP-ATP III) diagnostic criteria were used for the detection of metabolic syndrome. Written informed consent form was obtained from patients. Patients who were not volunteers, who were pregnant or lactating, diagnosed with cancer, chronic renal failure, chronic liver failure, and individuals using diuretic drugs were not included in the research. In the analyses of all hypothesis tests, p<0.05 was accepted significant. Results: The metabolic syndrome frequency was significantly higher in the GOUT group than in the ASH group (p<0.05). The difference between body mass index (BMI) values according to gender and groups was statistically significant among women (p<0.05). Mean body fat percentage values were significantly higher in women in both GOUT and ASH groups (p<0.05). Conclusion: The frequency of metabolic syndrome was significantly higher in the GOUT group. In addition, BMI and body fat percentage values were significantly higher in women. Abdominal obesity and possible hyperinsulinemia may cause more serious problems in the presence of hyperuricemia. Therefore, multiple parameters (various biochemical and anthropometric measurements) should be evaluated together. [ABSTRACT FROM AUTHOR]

Bilberry (Vaccinium myrtillus L.) is a fruit with high polyphenolic content and rich in anthocyanins. Due to its strong antioxidant capacity, it has potential effects in improving human health and reducing the risk of diseases. In addition to its antioxidant effect, it also possesses potential anti-inflammatory, anti-carcinogenic, anti-angiogenic, anti-proliferative, anti-atherogenic, anti-microbial, anti-diabetic, anti-lipidemic, neuroprotective, anti-metastatic, anti-radical effects, as well as preventing lipid oxidation, reducing oxidative stress and improving eye health. Bilberry consumption can potentially protect against and reduce the risks of chronic inflammation, dyslipidemia, hyperglycemia, increased oxidative stress, cardiovascular diseases, diabetes, dementia, and other age-related diseases and cancer. This review focuses on the potential mechanisms of action of bilberry in cancer. [ABSTRACT FROM AUTHOR]

The prevalence, incidence and mortality rates of neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease are gradually increasing. New approaches are being developed to manage the progression and treatment of neurodegenerative diseases. Catechins, polyphenolic compounds, are key compounds that demonstrate therapeutic effects with their properties such as antioxidant, anti-inflammatory, anti-apoptotic properties in the prevention and treatment of neurodegenerative diseases. The therapeutic effects of catechins have been exhaustively studied in human and animal models. Catechins can have anti-inflammatory effects by suppressing inflammatory pathways and cytokines, as well as antioxidant effects such as chelating metal ions and scavenging radicals. They might reduce phosphorylation of tau proteins, aggregation of amyloid-beta and apoptotic proteins release. They can also decrease alpha-synuclein accumulation and increase dopamine levels. With all these effects, they can have an effect on neurodegenerative diseases. This review points to the potential mechanisms of catechins in neurodegenerative diseases, based on their findings in the literature review. Catechins can reduce amyloid-β plaque aggregation and tau phosphorylation. Catechins can decrease alfa-synuclein levels. Catechins can protect neuronal cells with their anti-apoptotic effect. More comprehensive studies are needed to clarify this issue. [ABSTRACT FROM AUTHOR]