scholarly journals Fructose-Rich Diet Is a Risk Factor for Metabolic Syndrome, Proximal Tubule Injury and Urolithiasis in Rats

2021 ◽  
Vol 23 (1) ◽  
pp. 203
Author(s):  
Mariusz Flisiński ◽  
Andrzej Brymora ◽  
Natalia Skoczylas-Makowska ◽  
Anna Stefańska ◽  
Jacek Manitius
Keyword(s):  
Metabolic Syndrome ◽  
Uric Acid ◽  
Urinary Excretion ◽  
Proximal Tubule ◽  
Serum Insulin ◽  
Fractional Excretion ◽  
Urine Ph ◽  
Regular Diet ◽  
Male Wistar Rats ◽  
Excessive Consumption

Excessive consumption of fructose (FR) leads to obesity, metabolic syndrome (MS) and insulin resistance, which are known risk factors for kidney stones. The epidemiological study has suggested the association between fructose consumption and urolithiasis, but the precise mechanism is still not well understood. Male Wistar rats were assigned for 8 weeks to three groups with different FR content in diet: RD (n = 5)—regular diet with a FR < 3%; F10 (n = 6)—regular diet with an addition of 10% Fr in drinking water; F60 (n = 5)—60% FR as a solid food. Serum concentration of FR, creatinine (Cr), insulin (Ins), triglycerides (Tg), homocysteine (HCS), uric acid (UA), calcium (Ca), phosphate (Pi), magnesium (Mg) and sodium (Na) were measured. Based on 24 h urine collection the following tests were performed: urine pH, proteinuria (PCR), excretion of N-Acetyl-(D)-Glucosaminidase (NAG), monocyte chemoattractant protein (MCP-1), uric acid (uUAEx), phosphate (uPiEx), calcium (uCaEx), magnesium (uMgEx) and sodium (uNaEx). The creatinine clearance (CrCl) was calculated. Calcium deposits in kidney sections were examined using hematoxylin and eosin (HE) and von Kossa stains. The rats on F10 and F60, as compared to the RD diet, showed a tendency for lower CrCl, higher HCS level and some features of MS as higher Ins and TG levels. Interestingly, F10 (fluid) versus F60 (solid) diet led to higher serum Ins levels. F10 and F60 versus RD demonstrated higher urinary excretion of MCP-1 and NAG which were suggestive for inflammatory injury of the proximal tubule. F10 and F60 as compared to RD showed significantly lower uUAEx, although there were no differences in clearance and fractional excretion of UA. F60 versus RD induced severe phosphaturia (>30×) and natriuria (4×) and mild calciuria. F10 versus RD induced calciuria (3×), phosphaturia (2×) and mild natriuria. Calcium phosphate stones within the tubules and interstitium were found only in rats on FR diet, respectively, in two rats from the F10 group and another two in the F60 group. The rats which developed stones were characterized by significantly higher serum insulin concentration and urinary excretion of calcium and magnesium. A fructose-rich diet may promote development of calcium stones due to proximal tubule injury and metabolic syndrome.

Pathophysiology and Treatment of Uric Acid Stones

2018 ◽  
Author(s):  
Dustin Whitaker ◽  
Ava Saidian ◽  
Jacob Britt ◽  
Carter Boyd ◽  
Kyle Wood ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Metabolic Syndrome ◽  
Uric Acid ◽  
Urine Volume ◽  
Potassium Citrate ◽  
First Line ◽  
Urine Ph ◽  
Stone Composition ◽  
The Metabolic Syndrome ◽  
Uric Acid Stones

Uric acid is the third most common stone composition and comprises 7 to 10% of all kidney stones sent for analysis. These stones are more common with increasing age and in men. Uric acid stone disease is associated with conditions such as the metabolic syndrome and type 2 diabetes mellitus. Uric acid is produced by the enzyme, xanthine oxidase and is the final product of purine metabolism in humans. Three main factors contribute to the formation of uric acid stones: low urine pH (the most important), hyperuricosuria (rare, includes conditions such as myeloproliferative disorders and Lesch-Nyhan syndrome), and low urine volume. Uric acid stones appear radiolucent on plain radiographs and are ultimately diagnosed via stone analysis. These stones may be treated with medical expulsive therapy, dissolution therapy, or surgical intervention depending on the size, location, and clinical presentation. Urine pH manipulation therapy with potassium citrate is the first-line treatment for the prevention of uric acid stones and attempts at dissolution. Allopurinol should not be offered as the first-line therapy for uric acid stones.  This review contains 3 figures, 1 table and 38 references Key Words: ammonium, diabetes mellitus, epidemiology, management, metabolic syndrome, nephrolithiasis, pathophysiology, potassium citrate, uric acid, urine pH

scholarly journals Impact of Weight Loss on the Total Antioxidant/Oxidant Potential in Patients with Morbid Obesity—A Longitudinal Study

Antioxidants ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 376 ◽  
Author(s):  
Barbara Choromańska ◽  
Piotr Myśliwiec ◽  
Magdalena Łuba ◽  
Piotr Wojskowicz ◽  
Hanna Myśliwiec ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Uric Acid ◽  
Serum Insulin ◽  
Diagnostic Value ◽  
Morbidly Obese ◽  
Obese Patients ◽  
Antioxidant Power ◽  
Total Antioxidant ◽  
Ferric Reducing Antioxidant Power ◽  
Oxidant Status

The assessment of total antioxidant activity seems to have a higher diagnostic value than the evaluation of individual antioxidants separately. Therefore, this is the first study to assess the total antioxidant/oxidant status in morbidly obese patients undergoing bariatric surgery. The study involved 60 patients with Class 3 obesity (BMI > 40 kg/m2) divided into two equal subgroups: morbidly obese patients without and with metabolic syndrome. The analyses were performed in plasma samples collected before surgery as well as 1, 3, 6, and 12 months after a laparoscopic sleeve gastrectomy. Total antioxidant capacity (TAC), ferric-reducing antioxidant power (FRAP), DPPH (2,2′-diphenyl-1-picrylhydrazyl) radical assay, and total oxidant status (TOS) were significantly higher before surgery (as compared to the healthy controls, n = 60) and generally decreased after bariatric treatment. Interestingly, all assessed biomarkers correlated positively with uric acid content. However, the total antioxidant/oxidant potential did not differ between obese patients without metabolic syndrome and those with both obesity and metabolic syndrome. Only DPPH differentiated the two subgroups (p < 0.0001; AUC 0.8) with 73% sensitivity and 77% specificity. Plasma TAC correlated positively with body mass index, waist–hip ratio, serum insulin, and uric acid. Therefore, TAC seems to be the best biomarker to assess the antioxidant status of obese patients.

Allopurinol, rutin, and quercetin attenuate hyperuricemia and renal dysfunction in rats induced by fructose intake: renal organic ion transporter involvement

2009 ◽  
Vol 297 (4) ◽  
pp. F1080-F1091 ◽  
Author(s):  
Qing-Hua Hu ◽  
Chuang Wang ◽  
Jian-Mei Li ◽  
Dong-Mei Zhang ◽  
Ling-Dong Kong
Keyword(s):  
Metabolic Syndrome ◽  
Uric Acid ◽  
Renal Dysfunction ◽  
Rat Kidney ◽  
Organic Anion ◽  
Fractional Excretion ◽  
Prostaglandin E ◽  
Creatinine Ratio ◽  
Expression Levels ◽  
Rutin And Quercetin

Fructose consumption has been recently related to an epidemic of metabolic syndrome, and hyperuricemia plays a pathogenic role in fructose-induced metabolic syndrome. Fructose-fed rats showed hyperuricemia and renal dysfunction with reductions of the urinary uric acid/creatinine ratio and fractional excretion of uric acid (FEur), as well as other features of metabolic syndrome. Lowering serum uric acid levels with allopurinol, rutin, and quercetin increased the urinary uric acid/creatinine ratio and FEurand attenuated other fructose-induced metabolic abnormalities in rats, demonstrating that hyperuricemia contributed to the deficiency of renal uric acid excretion in this model. Furthermore, we found that fructose upregulated the expression levels of rSLC2A9v2 and renal-specific transporter (rRST), downregulated the expression levels of organic anion transporters (rOAT1 and rUAT) and organic cation transporters (rOCT1 and rOCT2), with the regulators prostaglandin E2(PGE2) elevation and nitric oxide (NO) reduction in rat kidney. Allopurinol, rutin, and quercetin reversed dysregulations of these transporters with PGE2reduction and NO elevation in the kidney of fructose-fed rats. These results suggested that dysregulations of renal rSLC2A9v2, rRST, rOAT1, rUAT, rOCT1, and rOCT2 contributed to fructose-induced hyperuricemia and renal dysfunction. Therefore, these renal transporters may represent novel therapeutic targets for the treatment of hyperuricemia and renal dysfunction in fructose-induced metabolic syndrome.

scholarly journals Association of Urine Findings with Metabolic Syndrome Traits in a Population of Patients with Nephrolithiasis

2021 ◽  
Author(s):  
Virginia L Hood ◽  
Kevan M Sternberg ◽  
Desiree de Waal ◽  
John R Asplin ◽  
Carley Mulligan ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Uric Acid ◽  
Calcium Oxalate ◽  
Protein Intake ◽  
Dietary Factors ◽  
Acid Excretion ◽  
Urine Ph ◽  
Stone Composition ◽  
Calcium Oxalate Stones ◽  
Net Acid Excretion

Background and objectives: The odds of nephrolithiasis increase with more metabolic syndrome (met-s) traits. We evaluated associations of metabolic and dietary factors from urine studies and stone composition with met-s traits in a large cohort of stone-forming patients. Design, setting, participants & measurements: Patients >18 years, who were evaluated for stones with 24 h urine collections, July 2009-December 2018, had records reviewed retrospectively. Patient factors, laboratory values and diagnoses were identified within 6 months of urine collection and stone composition within 1 year. Four groups with 0, 1, 2, > 3 met-s traits (hypertension, obesity, dyslipidemia, diabetes) were evaluated. Trends across groups were tested using linear contrasts in analysis of variance and analysis of covariance. Results: 1473 patients met inclusion criteria (835 with stone composition). Met-s groups were 0=684, 1=425, 2=211, 3 and 4 =153. There were no differences among groups for urine volume, calcium or ammonium (NH4) excretion. There was a significant trend (p<0.001) for more met-s traits being associated with decreasing urine pH, increasing age, calculated dietary protein, urine uric acid, oxalate, citrate, titratable acid (TAP), net acid excretion (eNAE) and uric acid supersaturation. The ratio of ammonium to net acid excretion did not differ among the groups. After adjustment for protein intake, the fall in urine pH remained strong, while the upward trend in TAP excretion was attenuated and NH4 decreased. Calcium oxalate stones were most common, but there was a trend for more uric acid (p<0.001) and fewer calcium phosphate (p=0.09) and calcium oxalate stones (p=0.01) with more met-s traits. Conclusions: Stone forming patients with met-s have a defined pattern of metabolic and dietary risk factors that contribute to an increased risk of stone formation including higher acid excretion, largely the result of higher protein intake, and lower urine pH.

scholarly journals Metformin reduces urate nephropathy in experimental nephrolithiasis

2017 ◽  
Vol 8 (4) ◽  
pp. 644-648
Author(s):  
V. Y. Perfil’ev ◽  
Y. F. Zverev ◽  
D. Y. Perfil’eva ◽  
I. V. Lysenko ◽  
A. G. Miroshnichenko
Keyword(s):  
Metabolic Syndrome ◽  
Classical Model ◽  
Free Radical Oxidation ◽  
Developed Countries ◽  
Ammonium Transport ◽  
Urine Ph ◽  
Lactate Dehydrogenase Activity ◽  
Radical Oxidation ◽  
Urate Nephropathy ◽  
Male Wistar Rats

The objective of the article is to evaluate the effectiveness of metformin in the prevention and treatment of experimental urate nephropathy. About 33% of the populations of developed countries suffers from metabolic syndrome. The relationship between metabolic syndrome, especially insulin resistance, with gout and urate nephrolithiasis, is now proven. The search for a common pathophysiological link in the development of these conditions allows us to identify insulin-dependent excessive urinary acidification due to impaired education and renal ammonium transport. We suggested the use of drugs that can increase the sensitivity of tissues to insulin, and induce a decrease in the manifestations of urate nephropathy. The study was performed on 30 male Wistar rats weighing 250–300 g. For the induction of urate nephropathy in rats, we used the classical model of inhibition of uricase by oxononium acid. Metformin was administered at a dose of 150 mg/kg in the treatment and prophylactic regimens. It was found that the use of metformin both in prophylactic and therapeutic regimen leads to a reliable decrease the level of uric acid in blood plasma and urine in rats with experimental urate nephrolithiasis. We found that the preventive use of metformin brought significant relief after experimental urate nephropathy, as evidenced by a shift in urine pH to the alkaline side, a decreased lactate dehydrogenase activity in urine, as well as a decrease in the processes of free radical oxidation in the blood and in the kidneys of the animals. 

The role of correction of hypogonadism in the treatment and prophylaxis of urolithiasis in the men presenting with metabolic syndrome

2015 ◽  
Vol 61 (2) ◽  
pp. 12-20
Author(s):  
D A Gusakova ◽  
S Yu Kalinchenko ◽  
A A Kamalov ◽  
Yu A Tishova
Keyword(s):  
Metabolic Syndrome ◽  
Uric Acid ◽  
Serum Uric Acid ◽  
The Body ◽  
Magnesium Concentration ◽  
Urine Ph ◽  
Testosterone Therapy ◽  
Serum Uric Acid Concentration ◽  
Group 1

Abdominal obesity is a major component of metabolic syndrome (MS) considered to be the key factor contributing to the development of testosterone deficiency (hypogonadism) in men. Bearing in mind the etiopathogenetic relationship between MS and urolithiasis (UL), the present study was undertaken for the purpose of elucidating the role of the main biochemical risk factors of metabolic syndrome in men, evaluating the influence of correction of hypogonadism on these factors, and optimization of the treatment and prevention of MS in these patients. The study included 90 men presenting with hypogonadism in whom the serum levels and renal excretion of the main lithogenic substances (uric acid, calcium, phosphates, magnesium) and urine pH were measured. At the first stage of the study, the patients were allocated to two groups. Group 1 was comprised of 52 patients with UL, group 2 consisted of 38 patients without UL. The patients of group 1 were found to suffer hyperuricemia (the serum uric acid levels 430 mcmol/l and higher). The patients of both groups exhibited hyperuricosuria (daily uric acid excretion over 4.13 mmol/24 hr) with the urine pH value of 5.5 and lower. The serum uric acid concentration was shown to positively correlate with the insulin and C-peptide levels. At the second stage of the study, 65 randomly selected patients were divided into two groups in one of which (n=40) they were given testosterone therapy. Compensation of hypogonadism in these patients was associated with a significant reduction of the serum uric acid levels and its daily excretion, an increase and normalization of urine pH, and a rise in the serum magnesium concentration, Similar significant changes of the same parameters were absent in the control subjects (n=25). Moreover, testosterone therapy improved characteristics of lipid and carbohydrate metabolism, caused reduction in the body weight, BMI, and the severity of insulin resistance.

High serum uric acid level and low urine pH as predictors of metabolic syndrome: a retrospective cohort study in a Japanese urban population

Metabolism ◽  
2012 ◽  
Vol 61 (2) ◽  
pp. 281-288 ◽  
Author(s):  
Shigeko Hara ◽  
Hiroshi Tsuji ◽  
Yuki Ohmoto ◽  
Kazuhisa Amakawa ◽  
Shiun Dong Hsieh ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Uric Acid ◽  
Cohort Study ◽  
Uric Acid Level ◽  
Retrospective Cohort ◽  
Urban Population ◽  
Acid Level ◽  
Serum Uric Acid Level ◽  
High Serum ◽  
Urine Ph

Urine electrolyte, mineral, and protein excretion in NHERF-2 and NHERF-1 null mice

2008 ◽  
Vol 294 (4) ◽  
pp. F1001-F1007 ◽  
Author(s):  
Rochelle Cunningham ◽  
Ali Esmaili ◽  
Eric Brown ◽  
Rajat S. Biswas ◽  
Rakhilya Murtazina ◽  
...  
Keyword(s):  
Uric Acid ◽  
Urinary Excretion ◽  
Proximal Tubule ◽  
Adaptor Proteins ◽  
Renal Proximal Tubule ◽  
Wild Type ◽  
Sodium Hydrogen Exchanger ◽  
Model Cell ◽  
Abundance And Distribution ◽  
Wild Type Control

The adaptor proteins sodium/hydrogen exchanger regulatory factor (NHERF)-1 and NHERF-2 have overlapping tissue distribution in renal cells and overlapping specificity in their binding to renal transporters and other proteins. To compare the kidney-specific differences in the function of these adaptor proteins, NHERF-1 and NHERF-2 null mice were compared with wild-type control mice. In NHERF-2 null mice, the renal proximal tubule abundance and distribution of NHERF-1 and NHERF-3 were not different from those in wild-type animals. The glomerular expression of podocalyxin and ZO-1 also did not differ. NHERF-1 null mice had increased urinary excretion of phosphate, calcium, and uric acid compared with wild-type control and NHERF-2 null mice. Because of the association between NHERF-2 and podocalyxin in glomeruli and ClC-5 in the renal proximal tubule, the urinary excretion of protein was determined. There were no differences in the urinary excretion of protein or low-molecular-weight proteins between wild-type control, NHERF-1−/−, and NHERF-2−/− mice. These studies indicate that the increased urinary excretion of phosphate and uric acid are specific to NHERF-1 null mice and highlight the fact that predictions about the role of adaptor proteins such as the NHERF proteins obtained from studies of model cell systems must be confirmed in whole animals.

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