(carbohydrate ≤ 20 g/day)
Note: data are from clinical trials that have been included in PubMed since 2012. A direct search was used to search for the following terms: “diet and uric acid” or “diet and gout” or “food and uric acid” or “food and gout”. A total of 462 articles were obtained. After following these exclusion criteria—repetitive articles, acute trials, dietary supplements, combination of drugs and food, questionnaire survey, exercise interference, and mismatched intervention subjects—a total of 32 articles showed the effect of diet on uric acid and other indicators of metabolic syndrome. ↑—increase; ↓—decrease; AA—amino acid; AUC—lower area under the curves; BG—blood glucose; BW—body weight; CRP— C -reactive protein; DASH—Dietary Approaches to Stop Hypertension; Ereq—energy requirement; HDL—high density lipoprotein; ICAM-1—intercellular cell adhesion molecule-1; LDL—low density lipoprotein; MDA—malondialdehyde; MS—indicators of metabolic syndrome; OR—odds ratio; PUA—plasma uric acid; SUA—serum uric acid; TBARS—thiobarbituric acid reactive substance. TC—total cholesterol; TG—triglyceride; UAM—indicators of uric acid metabolism; UUA—urine uric acid.
3.1.1. high fat.
Dietary fat is primarily metabolized into triglycerides within intestines and packaged as chylomicrons for delivery to peripheral tissues, where adipocytes further transfer triglycerides into free fatty acids (FFAs) for energy uptake and storage [ 67 ]. A small amount of FFAs can be absorbed by the liver tissue, together with lipids remaining in the chylomicron [ 67 ]. High-fat foods can evoke the pleasure of eating and promote the individual’s desire to consume more energy-dense diets [ 68 ], which culminates in the overproduction of FFAs. Free fatty acids-mediated metabolic events initiate acute onset of gouty disease in the presence of MSU crystals deposited in the joint. The interaction of FFAs with TLR2 synergized with MSU crystals leads to the release of IL-1β induced by ASC/caspase 1 [ 69 ].
High fat consumption can cause excessive accumulation of triglycerides, inducing increased fat mass and obesity. It has been reported that overweight/obesity was connected with 60% of hyperuricemia cases in a clinical trial of 14,624 adults [ 70 ], possibly due to lipid metabolic disorder promoting purine metabolism by elevating XO activity [ 71 ]. Hypertrophy and hyperplasia of adipocytes are associated with higher oxygen consumption, which evokes hypoxic damage in other tissues, resulting in the chronic inflammation of obesity [ 72 ]. Nonalcoholic fatty liver disease and nonalcoholic fatty pancreatic disease subsequently occur when lipid overload occurs in the liver and pancreatic tissue, causing metabolic dysfunction in both and affecting acid-base balance. Metabolic acidosis further promotes hypercalciuria, low urine pH and hypocitraturia, predisposing patients to MSU crystal deposition and calcium renal stone formation [ 73 ]. In response to excessive FFAs circulation, insulin secreted from pancreatic β-cells upregulates the expression of renal urate transporters, including GLUT9 and URAT1, and decreases ABCG2 levels, promoting high SUA levels [ 18 ]. Uric acid conversely induces lipid accumulation and insulin resistance (IR), thereby forming a vicious cycle of uric acid and insulin [ 74 ].
Prior to the onset of IR and obesity, high fat intake has been found to upregulate the expression of reactive oxygen species (ROS) in adipose tissue and liver, along with the metabolic disturbance of adipocytes and the dysregulation of adipokine release [ 75 ], promoting or aggravating MSU-mediated NF-κB-dependent inflammation. For example, leptin levels secreted from adipose tissues were elevated in patients with gouty inflammation, and leptin can facilitate MSU-induced acute gout-related proinflammatory cytokine production in macrophages and synoviocytes [ 76 ]. The key adipocyte-derived chemokines McP-1 and LTB4 recruit proinflammatory macrophages to induce inflammation amplification, thus aggravating gouty inflammation [ 77 ]. Furthermore, a high-fat diet changes gut microbiota composition, leading to reduced microbiota diversity and an increased ratio of Firmicutes to Bacteroidetes and to the reduction of microbiota-derived beneficial metabolites such as butyric acid, which further aggravates gouty arthritis [ 20 ].
Sugars are the most abundant macromolecules in nature and can be classified according to their structure into monosaccharides, complex carbohydrates, and glycoconjugates [ 78 ]. They are the primary carbon source for ATP production and cellular biosynthesis. Sugars from diets can be absorbed as glucose, galactose or fructose in the liver portal circulation. The liver and gut normally process galactose and fructose into lactate, glucose and organic acids through gluconeogenesis, glycogenolysis, aerobic oxidation and other pathways [ 78 ]. High sugar consumption might initiate metabolic disease processes accompanied with hyperglycemia, IR, and fat accumulation. Moreover, high sugar intake in obese patients increases serum urate and decreases the percent of uric acid to creatinine clearance, indicating a close association between hyperuricemia and a high sugar diet [ 79 ]. Sugar-sweetened beverages containing high-fructose corn syrup and sucrose or almost equal amounts of fructose and glucose, which account for approximately one-third of added sugar consumption in the diets of American adults [ 80 ], have been thought to be closely connected with a high prevalence of hyperuricemia in Western countries [ 81 ]. Long-term high sugar consumption has been found to accelerate the accumulation of uric acid and promote MSU deposition in fly renal tubules, suggesting that a similar problem may occur in human excretory systems under dietary challenges [ 82 ]. In a follow-up study of 650 participants, the results confirmed that a high-sugar diet participates in kidney dysfunction and uric acid metabolism disorders [ 82 ].
The metabolic effects of sugar are distinct from those of starch principally because of the fructose component. Studies of dietary sugar intervention in animals and humans have demonstrated that overconsumption of fructose, but not glucose, can manifest multiple traits of metabolic syndrome [ 83 , 84 , 85 ], indicating that fructose might be responsible for high sugar-driven hyperuricemia and gout [ 86 ]. Fructose metabolism starts within the small intestinal tissue, where fructose can be absorbed by the facilitative hexose transporter GLUT5 (SLC2A5) and converted by ketohexokinase. Notably, exposure to high fructose increases the intestinal villus length to expand the surface area of intestinal cells that can absorb more nutrients from food [ 87 ], possibly aggravating high fructose-mediated metabolic disorders via overconsumption of nutrients. Excessive fructose consumption-induced gouty syndrome is related to the altered gut microbiota and its metabolites and induces inflammation and fatty acid disorders. Since high fructose intake induces the proliferation of mucus-degrading bacteria in the gut microbiota, decreased mucus glycoproteins can promote intestinal barrier damage and pathogen invasion [ 88 ].
Fructose-derived metabolites can be transferred from the intestinal tissues to the liver and systemic circulation, and the redundant fructose can also directly reach the hepatic tissue or enter the systemic circulation when the intestinal clearance capacity reaches an upper limit [ 89 ]. Fructose culminates the main rate-limiting step of glycolysis and is rapidly converted into ketohexokinase to generate fructose-1-phosphate, which is further metabolized into glyceraldehyde 3-phosphate and dihydroxyacetone phosphate. The acute fructose overload in the liver leads to ATP degradation and a decrease in ATP synthesis, both of which lead to an increase in AMP levels and stimulation of AMP deaminase activity, subsequently accelerating the formation of uric acid with consequent hyperuricemia. More notably, the costly fructose metabolism can also result in renal inflammation and fibrosis and form kidney stones due to calcium salt precipitation in high-fructose diet-fed mice [ 90 ]. Alarmingly, a normal physiological concentration of fructose in the kidney still causes a risk of defective elimination of uric acid and activation of renal inflammation by increasing the expression of intercellular adhesion molecule-1 in the serum and endothelial cells [ 91 ]. Therefore, carbohydrate restrictions, especially fructose intake, have been regarded as an efficient diet intervention for gouty patients to modulate the disease state. It has been shown that the intake of fructose-rich fruits could bring about a temporary upregulation of uric acid. However, the moderate consumption of these foods over a long time can facilitate the excretion of uric acid, which could be correlated with the alkalization of body fluids [ 92 ]. Therefore, it is always suggested that limiting fructose-rich soft drinks or reducing the consumption of high-fructose drinks rather than fruits is better for gout improvement.
Proteins are biomacromolecules formed by folding long chains of amino acids, and dietary protein digestion in the gastrointestinal tract can provide amino acid dipeptides and tripeptides for cellular metabolism and protein synthesis in muscle or other tissues. High protein consumption is well known for its promotion of energy expenditure and urea synthesis. In addition, high dietary protein intake can also affect uric acid homeostasis, since protein digestion can generate several amino acids, such as glutamine, glycine and threonine, to induce purine synthesis, promoting the development of hyperuricemia [ 93 ]. A cohort study with 193,676 participants further revealed that higher nondairy animal protein consumption results in a disturbance of uric acid metabolism, including a reduced level of citrate and a higher level of uric acid and acidic urine, which subsequently promotes uric acid stone formation [ 94 ]. In addition, long-term high dietary protein intake has been shown to have adverse effects on uric acid elimination due to increased intraglomerular pressure and flow in kidney tissues [ 95 ]. The severity of glomerular damage has been significantly attributed to elevated SUA levels; hence, dietary recommendations for gouty patients often suggest that excessive protein intake should be restricted to avoid placing kidney tissue under undue stress.
Studies have also shown inconsistent effects of dietary proteins from different sources [ 96 ]. Overconsumption of animal proteins is linked to an elevated prevalence of gout, whereas overconsumption of plant protein (soybeans and soy products) or dairy product intake are associated with a reduced risk [ 8 , 96 ]. When compared with foods rich in plant proteins, an animal protein-rich diet promotes acidic urine production and uric acid stone formation [ 94 ]. Conversely, substitution of plant-based protein for a carbohydrate-rich diet can attenuate IR and compensatory hyperinsulinemia [ 97 ], thus improving the renal clearance of urate. Therefore, choosing appropriate dietary protein sources and controlling the amount of protein intake might represent an effective intervention for the improvement of gouty diseases.
3.2.1. vitamins.
Vitamins are essential trace elements that act as regulators of physiological and pathological functions, such as participating in immune responses, antioxidant activities and redox reactions. It has been demonstrated that an adequate intake of vitamin supplements or consumption of vitamin-rich fruits and vegetables seems to be a valid approach for hyperuricemia and gout treatment. Vitamins such as vitamin A, vitamin E, and vitamin C show beneficial effects against oxidative stress and inflammation, as well as effectively decreasing SUA levels [ 98 , 99 , 100 ], and the same uric acid-lowering effect also appears in a vitamin D-rich diet [ 101 ]. Additionally, vitamin E is also considered a membrane stabilizer that inhibits MSU crystal-induced hemolysis [ 102 ]. Many studies performed in humans and animals have shown that vitamin C (l-ascorbic acid) consumption can affect uric acid reabsorption and excretion to reduce SUA levels [ 100 ]. Both uric acid and vitamin C can be reabsorbed in the proximal tubule via anion-exchange transport, and vitamin C overload can competitively suppress the reabsorption of uric acid [ 103 ] in the filtrate. Meanwhile, its downregulation of URAT1 activity and/or Na + -dependent anion cotransporter could promote uric acid excretion [ 100 ]. The uricosuric function of vitamin C also appears to directly act on the glomerulus by reducing glomerular microvascular ischemia and increasing afferent arteriole dilation, thus increasing the glomerular uric acid filtration rate [ 104 ]. Furthermore, vitamin C reduces the incidence of gout by alleviating the NF-κB/NLRP3-related inflammatory response to MSU deposition [ 105 ].
Minerals, including potassium, zinc, calcium, copper, iron, and selenium are micronutrients that are essential for body metabolism [ 73 ], and deficiencies or excesses of these micronutrients are potentially hazardous occurrences that might be involved in the development of gout. It is well known that dietary potassium consumption has obvious diuretic and natriuretic effects, and even a minor potassium insufficiency triggers an impairment in the kidney’s capacity to secrete sodium chloride and retain sodium [ 106 ], resulting in renal dysfunction, while long-term routine potassium replenishment aggravates thiazide diuretic-mediated elevation of uric acid [ 107 ]. A similar facilitation effect was observed when iron accumulation triggers increased saturated transferrin-mediated XO activity [ 108 , 109 ]. Minerals also have a crucial role in maintaining acid-base balance. This has been attributed to keeping urine electrically neutral by regulating the secretion of anions such as chloride, sulfate, and phosphate in kidney tissues [ 73 ]. For instance, urinary calcium loss is a crucial risk factor that can trigger calcium stone formation and cause a uric acid excretion disorder [ 73 ]. Normal calcium intake can decrease the potential risk of kidney stone formation and is conducive to uric acid elimination in renal tissue [ 110 , 111 ].
Dietary fibers refer to plant-derived carbohydrates that are resistant to hydrolyzation or assimilation in the upper gastrointestinal tract, and fibers trapped in the gut can increase intestinal viscosity and satiety, as well as reduce gastric emptying rate and regulate intestinal conduction [ 112 ]. Correspondingly, dietary fibers reduce the intake and absorption of high-energy food [ 113 ]. The consumption of dietary fibers can manage glucose and lipid metabolism to regulate energy balance [ 113 , 114 ]. More importantly, a lack of these fibers leads to a slower recovery of gut dysbiosis, and dietary fiber supplementation is able to improve the composition of the gut microbiota [ 115 ], suggesting a close connection between fiber and intestinal flora disorder in gout patients. The fiber fermentation process by gut microbiota accompanies the release of microbiota-driven metabolites (short-chain fatty acids, SCFAs) that show beneficial effects on the host’s health [ 116 ]. After dietary fiber intake, acetate is the most abundant microbiota-derived SCFAs in the blood and can quickly resolve MSU-induced inflammation by promoting caspase-dependent apoptosis of neutrophils and the excretion of the anti-inflammatory IL-10 against LPS-induced inflammation [ 31 ]. Butyrate is another SCFAs mainly produced by microbiotal fermentation of indigestible fibers, and has been shown to improve lipid accumulation in the liver and pancreas, thereby reducing uric acid metabolism abnormalities by XO activation [ 71 ]. Butyrate can also decrease the activation of NF-κB induced by LPS and the translation or transcription of IL-1β by inhibiting histone deacetylases in human peripheral blood mononuclear cells [ 117 ]. Therefore, the consumption of more fiber-rich whole grains, vegetables and fruits is beneficial for regulating gastrointestinal homeostasis, reducing the intake of unhealthy foods and reshaping the gut microbiota. Meanwhile, the salutary metabolites produced by the microbiota-induced digestion of dietary fiber can regulate the inflammatory state of gouty patients and reduce uric acid production, all of which are conducive to the management of gout.
The close association of specific foods with SUA levels, as shown in Table 1 , illustrates that the essential impact of food on health is ascribed to the synthesized effects of the nutrients from food, specifically the dominant or beneficial nutritional factors determining the final performance. Taking dairy products as an example, the increased intake of dairy products, especially those with low fat, can reduce the incidence of gout [ 8 ]. Late season skim milk, which contains higher levels of orotic acid than early season skim milk, has a preferential impact on the excretion of uric acid [ 118 ]. Moreover, glycomacropeptide and G600 milk fat addition in skim milk can greatly and effectively relieve joint pain and the frequency of gout flares [ 119 ].
The dietary management for gouty patients is commonly self-prescribed and centers around the control of purine sources, such as reduced consumption of purine-rich foods, which theoretically attenuates uric acid production; but patients often fail to adhere to recommendations in the long term due to the limited palatability of purine-free diets [ 34 , 37 ]. Although piecemeal modifications of the various yet limited numbers of nutrients often provide incomplete dietary recommendations [ 34 ], attention should be given to nutrient richness and structure to avoid the burden of inappropriate dosage. For example, the plasma concentrations of vitamin C saturation ranges daily from 200 to 400 mg, implying that exceeding the recommended supplemental dose has little effect on the consequences [ 120 ]. More importantly, taking high-dose and long-term supplements of vitamin C may be associated with adverse effects, and the resulting excessive uric acid excretion could elevate the risk of kidney stones in gouty patients [ 121 , 122 ]. As shown in Figure 3 , recommended nutritional interventions should emphasize the necessity for appropriate supplementation of plant-derived fibers and dairy-derived protein and persuade patients to avoid high-compensation consumption of refined saturated fats and carbohydrates [ 34 ]. The typical dietary patterns include a DASH and Mediterranean diet, both of which are comprised of fruits, vegetables, and low-fat dairy products with reductions in total and saturated fats. Increasing evidence supports that consuming a DASH diet can continuously attenuate SUA in hyperuricemia patients and reduce the incidence of gout in participants [ 34 , 45 ]. Similar SUA-lowering effects have been observed in a research investigations of the Mediterranean diet [ 58 ]. Moreover, intervention with the DASH diet combined with adequate sodium and plant-derived protein shows more beneficial functions in reducing SUA levels [ 33 , 37 ].
Recommended food-derived nutritional interventions with anti-gouty mechanisms. Dietary management recommendations for gout patients include appropriate intake of fiber, minerals, and vitamins, as well as the selection of high-quality sugars, fats, and proteins, which are usually of plant origin. In addition, the consumption of products containing probiotics helps regulate intestinal homeostasis in patients with gout. ↑—increase; ↓—decrease; →—maintain; UA—uric acid; HQ—high-quality.
Most cases of dietary management related to uric acid reduction are reported in the nongouty population (as shown in Table 1 ). Dietary modification against gouty disease is commonly selected as an adjunct therapeutic strategy with medicinal drug therapy [ 10 ]; however, clinical trial data on the effects of dietary modifications combined with pharmacological interventions on gout are mostly lacking, as shown in Table 2 . By way of illustration, colchicine and nonsteroidal anti-inflammatory agents (NSAIDs) have been used to treat acute gouty inflammation. Their combined use with dietary micronutrient supplementation can remedy micronutrient deficiency induced by NSAIDs and colchicine [ 123 , 124 ]. Allopurinol, a first-line drug used as a xanthine oxidase inhibitor against gout, requires high protein replenishment to facilitate renal clearance [ 125 ]. Therefore, our recommendation is for individuals to follow a healthy diet for prevention purposes, and for patients with mild gout, we recommend the DASH and Mediterranean diet, which focus on plant-based components. Additionally, we recommend a reduction in the consumption of high-fat foods (fast food and cream products), especially foods with trans fatty acids (such as margarine and butter), and for individuals to pay attention to the amount of nutrient supplements consumed. For patients with severe gout, dietary modification and medication should be combined, and health care providers should remind patients of food–drug interactions to achieve synergistic effects.
Combination of nutrition modification and drug supplementation.
Medicine | Dietary Intervention | Participants | Time | Major Findings |
---|---|---|---|---|
Lesinurad [ ] | High-fat and high-calorie meal | 16 healthy men (ages 18 to 55 years) | 6 days | •C ↓ vs. the fasted phase •serum urate-lowering effect and renal clearance ↑ vs. the fasted phase •absorption was slightly delayed vs. fasted phase |
Lesinurad [ ] | Moderate-fat diet | 16 nonobese men (ages 18 to 55 years) | 10 days | •T 4 h delay •C ↓ in the fed state vs. the fasted phase |
Colchicine [ ] | Seville orange juice or grapefruit juice | 44 nonobese adults (ages 18 to 45 years) | 4 days | •C and AUC ↓ in the seville orange juice group vs. the nonjuice group •T occurred 1 h delay compared with in the seville orange juice group vs. the nonjuice group |
Febuxostat [ ] | High-fat breakfast | 68 healthy adults (ages 18 to 55 years) | Not specified | •C and AUC ↓ under feeding conditions vs. fasting conditions •SUA concentrations ↓ after treatment with febuxostat (80 mg) |
Etoricoxib [ ] | High-fat meal | 12 healthy adults (ages 50 to 64 years) | 10 days | •the rate of absorption ↓ in the fed phase vs. the fasted phase •T occurred with an approximately 2 h delay in the fed phase vs. the fasted phase |
Allopurinol/oxipurinol [ ] | High-protein or low-protein diet | 6 healthy adults (ages 20 to 30 years) | 28 days | •plasma AUC significantly ↑ in the high-protein diet group •renal clearance significantly ↓ in the high-protein diet group |
Allopurinol [ ] | Low-purine diet | 60 hypertensive patients with high SUA levels (average age of 54.4 years) | 36 weeks | •SUA significantly ↓ in the intervention groups •6 months after the intervention, SUA shows an elevation tendency in the low-purine diet + medication group and medication-only group •6 months after the intervention, SUA shows a continuous drop in the low-purine diet group |
Note: Data are from clinical trials that have been included in PubMed. A direct search was used to search for the following terms: “diet” or “food” with “drug” or “medicine” or “treatment” with “gout” or “hyperuricemia”; “diet” or “food” with commonly used clinical anti-gout drugs including “zurampic (lesinurad)”, “colchicine”, “febuxostat”, “allopurinol”, “probenecid”, “aspirin”, “pegloticase”, “benzbromarone” and “etoricoxib”. A total of 751 articles were obtained. After following these exclusion criteria—repetitive articles, dietary supplements, drug interactions, formulation improvement, exercise interference, nonmarket food and mismatched intervention subjects—a total of 7 articles showed the effect of the combination of diet and medication in the treatment of gout. ↑—increase; ↓—decrease; AUC—area under curve; C max —maximal plasma concentration; SUA—serum uric acid; T max —time to reach C max .
Our study has shown the important role of diet in gout development and management and how dietary adjustments based on nutrient composition should be an important component of routine care for gout. Gout patients are commonly prone to choose health management by dietary modification because diet changes can instantly affect gout flares via multiple signaling pathways. Diet-induced systemic metabolic pathways, including purine, lipid, and glucose metabolism, as well as energy balance and gut microbiota changes, have provided new mechanistic insights and potential interventions for gout progression. Since foods are eventually metabolized into multiple nutrients for metabolic homeostasis in the body, dietary modification might represent an appropriate nutritional regulation for gout patients or for potential patients to effectively reduce the incidence of gout. The critical role of nutritional factors on gout development also supported the following recommended nutritional modification strategies: (1) reducing nutritional risk factors against metabolic syndrome; (2) supplementing with beneficial nutrients to affect uric acid metabolism and gouty inflammation; and (3) considering nutritional modification combined with medication supplementation to decrease the frequency of gout flares. Our consistent principle is that, in terms of diet, nutritional balance should be analyzed from the point of view of enrichments and structures of nutritional elements. Evidence supports that a low-fat, low-carb, plant-based dietary intervention is suitable for gouty patients; however, we need to pay specific attention to the golden rule of healthy dietary intake, that is, moderation. In addition, we advocate the combination of medications and dietary modification for gouty patients in therapy, and caution that they should note the impact of nutritional factors on drug pharmacokinetics and pharmacodynamics. However, many human studies focusing on the relationship of food and SUA levels often do not involve gouty patients. A limited number of clinical research studies explore food/nutrition and gout or anti-gout drugs, resulting in limited being drawn conclusions. In conclusion, the dietary mechanisms and nutritional basis provide scientific evidence for the prevention and improvement of gouty diseases, and dietary modifications based on effective regulatory mechanisms may be a promising strategy to reduce the high prevalence of gout.
We would like to thank Peili Rao, Yannan Zheng and Yijie Song, for their revision suggestions of figures.
This research was funded by the Key-Area Research and Development Program of Guangdong Province (2020B1111110003).
Y.X. and H.X. initiated the idea and performed the study. Y.Z. and S.C. wrote the manuscript. Y.Z., S.C., M.Y., Y.X. and H.X. discussed and revised the manuscript. H.X. has final responsibility for all parts of this manuscript. All authors have read and agreed to the published version of the manuscript.
Not applicable.
Data availability statement, conflicts of interest.
The authors declare no conflict of interest.
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In this paper, we present and discuss how the acid rain problem became a key environmental issue among industrial countries from the late 1960s and the following decades (Fig. 2).We view the problem from a science-to-policy interaction perspective, based on a Symposium in Stockholm in the autumn 2017 organised to manifest 50 years of international air pollution science and policy development.
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The term 'acid rain' refers to atmospheric deposition of acidic constituents that impact the earth as rain, snow, particulates, gases, and vapor. Acid rain was first recognized by Ducros (1845) and subsequently described by the English chemist Robert Angus Smith (Smith, 1852) whose pioneering studies linked the sources to industrial emissions and included early observations of deleterious ...
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Acid rain, linked to fossil fuel-burning emissions, featured prominently in 1970 s to 1990 s headlines. Concern over dying lakes triggered international solution seeking, but as emissions-reducing agreements were enacted, attention to the problem faded. ... Since 1968, this research hub, renowned for experimental manipulations of whole lakes ...
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The amount and strength of base for ZrO2 and Mg(OH)2 catalysts in hot compressed water at 380 °C and 30 MPa were investigated. The effect of acid poisoning on the rate of 2,5-hexanedione cyclization, which was used as an indicator of acid adsorption on base sites, was analyzed by using the Langmuir equation, and differences in basicity between both catalysts were discussed. Both catalysts ...
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Gout is well known as an inflammatory rheumatic disease presenting with arthritis and abnormal metabolism of uric acid. The recognition of diet-induced systemic metabolic pathways have provided new mechanistic insights and potential interventions on gout progression. However, the dietary recommendations for gouty patients generally focus on ...