Abstract:Background:The present study investigated the role of synergistic interaction between hyperuricemia and abdominal obesity as a risk factor for the components of metabolic syndrome. Methods: We performed a cross-sectional study using the data of 16,094 individuals from the seventh Korean National Health and Nutrition Examination Survey (2016 to 2018). The adjusted odds ratios of metabolic syndrome and its components were analyzed by multivariate logistic regression analysis. The presence of synergistic interact… Show more
“…Mice body weights in the HF group were significantly higher than those in the other three groups, consistent with the established relationship between a high-fat diet and the accumulation of body weights. , However, our experiment showed that uric acid was not positively correlated with serum lipids. This finding is inconsistent with those of some previous studies, which suggested that hyperuricemia can lead to elevated lipid levels and ectopic fat deposition. ,, However, uric acid has excellent antioxidant properties at low concentrations − and only functions as a pro-oxidant at high concentrations, which is harmful to the body .…”
Section: Discussionsupporting
confidence: 88%
“…27−29 Moreover, a high uric acid diet causes elevated blood lipids. 30,31 These results confirm that there is a mutual promotion between uric acid and blood lipids. 32 However, it is not clear whether high uric acid combined with high lipid levels has a reinforcing effect on PS.…”
Section: ■ Introductionsupporting
confidence: 64%
“…35,36 However, there were no differences in the mRNA expression level of PLA2G2A among groups, suggesting that other genes may be involved in the regulation of PLA2G2A. Most studies have shown [28][29][30][31]43 that there is a degree of interaction between SUA and lipids and that uric acid has negative health effects. However, the results in this study revealed that low concentrations of SUA inhibit fat accumulation.…”
Section: ■ Discussionmentioning
confidence: 97%
“…Several studies have shown that low uric acid levels damage the nervous system, , whereas high uric acid levels exert protective effects . Many studies have suggested that high-fat diets cause elevated uric acid levels in addition to elevated blood lipids. − Moreover, a high uric acid diet causes elevated blood lipids. , These results confirm that there is a mutual promotion between uric acid and blood lipids . However, it is not clear whether high uric acid combined with high lipid levels has a reinforcing effect on PS.…”
Background: despite evidence for mutually reinforcing effects of serum uric acid (SUA) and lipids, the effects of uric levels on pancreatic steatosis are not well-established. In this study, the relationship between low concentrations of uric acid and pancreatic steatosis was evaluated. Methods: forty C57BL/6J mice were fed a diet of high uric acid (HU), high fat (HF), high uric acid and high fat (HUHF), and normal control (NC) (10 mice in each group). Weight was measured weekly. Ultrasonography was performed to observe the pancreatic echo intensity of all mice before the end of feeding. Subsequently, peripheral blood was taken for biochemical examination. Intact pancreatic tissues were taken, part of which was used for pathological examination, part of which was used for PCR experiments and Western Blot experiments to obtain glycerophospholipid-associated mRNA data and protein levels. Results: body weight was significantly higher in the HF group than in the other three groups. Higher uric acid matched lower total cholesterol and triglyceride, matched higher low-density lipoprotein, and matched equal high-density lipoprotein. Ultrasound images and HE staining of pancreatic tissues of mice showed that higher uric acid matched lower fat content. The mRNA levels of phospholipase A2 group IB were highest in high uric acid group, while relative protein expression levels were lowest in high uric acid and control groups. Phospholipase A2 group IIA showed the opposite patterns. Conclusions: elevated serum uric acid at low concentrations can inhibit pancreatic steatosis, which is modulated via the glycerophospholipid metabolic pathway.
“…Mice body weights in the HF group were significantly higher than those in the other three groups, consistent with the established relationship between a high-fat diet and the accumulation of body weights. , However, our experiment showed that uric acid was not positively correlated with serum lipids. This finding is inconsistent with those of some previous studies, which suggested that hyperuricemia can lead to elevated lipid levels and ectopic fat deposition. ,, However, uric acid has excellent antioxidant properties at low concentrations − and only functions as a pro-oxidant at high concentrations, which is harmful to the body .…”
Section: Discussionsupporting
confidence: 88%
“…27−29 Moreover, a high uric acid diet causes elevated blood lipids. 30,31 These results confirm that there is a mutual promotion between uric acid and blood lipids. 32 However, it is not clear whether high uric acid combined with high lipid levels has a reinforcing effect on PS.…”
Section: ■ Introductionsupporting
confidence: 64%
“…35,36 However, there were no differences in the mRNA expression level of PLA2G2A among groups, suggesting that other genes may be involved in the regulation of PLA2G2A. Most studies have shown [28][29][30][31]43 that there is a degree of interaction between SUA and lipids and that uric acid has negative health effects. However, the results in this study revealed that low concentrations of SUA inhibit fat accumulation.…”
Section: ■ Discussionmentioning
confidence: 97%
“…Several studies have shown that low uric acid levels damage the nervous system, , whereas high uric acid levels exert protective effects . Many studies have suggested that high-fat diets cause elevated uric acid levels in addition to elevated blood lipids. − Moreover, a high uric acid diet causes elevated blood lipids. , These results confirm that there is a mutual promotion between uric acid and blood lipids . However, it is not clear whether high uric acid combined with high lipid levels has a reinforcing effect on PS.…”
Background: despite evidence for mutually reinforcing effects of serum uric acid (SUA) and lipids, the effects of uric levels on pancreatic steatosis are not well-established. In this study, the relationship between low concentrations of uric acid and pancreatic steatosis was evaluated. Methods: forty C57BL/6J mice were fed a diet of high uric acid (HU), high fat (HF), high uric acid and high fat (HUHF), and normal control (NC) (10 mice in each group). Weight was measured weekly. Ultrasonography was performed to observe the pancreatic echo intensity of all mice before the end of feeding. Subsequently, peripheral blood was taken for biochemical examination. Intact pancreatic tissues were taken, part of which was used for pathological examination, part of which was used for PCR experiments and Western Blot experiments to obtain glycerophospholipid-associated mRNA data and protein levels. Results: body weight was significantly higher in the HF group than in the other three groups. Higher uric acid matched lower total cholesterol and triglyceride, matched higher low-density lipoprotein, and matched equal high-density lipoprotein. Ultrasound images and HE staining of pancreatic tissues of mice showed that higher uric acid matched lower fat content. The mRNA levels of phospholipase A2 group IB were highest in high uric acid group, while relative protein expression levels were lowest in high uric acid and control groups. Phospholipase A2 group IIA showed the opposite patterns. Conclusions: elevated serum uric acid at low concentrations can inhibit pancreatic steatosis, which is modulated via the glycerophospholipid metabolic pathway.
“…According to epidemiological surveys, the prevalence of HUA in Chinese adults remarkably rises from 8.4% in 2009–2010 to 14.0% in 2018–2019, and also more than 20.0% from 2007 to 2016 in United States ( 7 , 8 ). Although the serum UA level is not a diagnostic criterion for MetS, longitudinal studies have demonstrated that HUA is closely associated with the development of MetS and its components, and there is a bidirectional relationship between them ( 9 , 10 ). The morbidity of MetS gradually raises with the growth of serum UA level ( 11 ).…”
Ferulic acid is a well-known phenolic acid compound and possesses multiple health-promoting and pharmacological effects. Metabolic syndrome (MetS) and hyperuricemia (HUA) have become health problems worldwide and are closely connected. The aim of this study was to explore the influence of ferulic acid on MetS-related HUA and its underlying mechanisms. Rats were administered high-fructose and high-fat diet (HFFD) with or without ferulic acid (0.05 and 0.1%) for 20 weeks. Intake of HFFD resulted in obesity, hyperglycemia, insulin resistance, and dyslipidemia, which were alleviated by ferulic acid consumption. Treatment of rats with ferulic acid diminished the levels of lipids and inflammatory cytokines and enhanced the activities of antioxidant enzymes in the liver caused by HFFD. Additionally, administration of ferulic acid blocked a HFFD-induced elevation in activities and mRNA expression of enzymes involving in uric acid (UA) synthesis. Molecular docking analysis denoted that ferulic acid bound to the active center of these enzymes, indicative of the potential interaction with each other. These two aspects might partially be responsible for the decrement in serum UA content after ferulic acid ingestion. In conclusion, ferulic acid supplementation ameliorated lipid and glucose metabolic abnormalities, hepatic damage, and UA formation in MetS rats. There was a dose correlation between lipid deposition and UA synthesis-related indicators. These findings implied that ferulic acid could be applied as a promising dietary remedy for the management of MetS-associated HUA.
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