We studied 14 patients (11 women and 3 men) from 18 to 33 years old, suffering from type I diabetes mellitus with normal renal function (creatinine clearance 106.91 +/- 28.73 ml/min) and serum uric acid below 2.5 mg/dl (2.34 +/- 0.11 mg/dl) as well as a high uric acid clearance (23.04 +/- 5.92 ml/min) and fractional urate excretion (21.4 +/- 2.6) versus urate clearance 9.82 ml/min and fractional urate excretion 8.80 +/- 1.3 in 14 normal control subjects. The study of the uricosuric mechanisms was conducted by the combination of probenecid (PB) test which inhibits the reabsorption of secreted urate, and pyrazinamide (PZA) test, which inhibits its tubular secretion. The results of studies indicate that the increase in urate clearance was accounted for by increased PZA-nonsuppressible urate suggesting a decreased reabsorption of filtered urate. Increased PZA-suppressible urate excretion combined with impaired response to a uricosuric drug is consistent with impaired reabsorption of secreted urate. According to our findings, increased urate excretion in diabetic patients may be attributed to the inhibition of both filtered and secreted reabsorption. This reabsorptive tubular abnormality is consistent with the view of an interference of tubular reabsorption of glucose with the tubular capacity for uric acid reabsorption.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1159/000186512 | DOI Listing |
Biochem Biophys Res Commun
January 2025
Department of Biopharmaceutics, School of Pharmacy, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan. Electronic address:
SLC17A3 localized to the apical membrane of the renal proximal tubules has been implicated in the urinary excretion of drugs and endogenous/exogenous metabolites transported into the tubules by OAT1 and OAT3. Because SLC17A3 mediates the facilitated diffusion of organic anions, which requires a sensitive and rapid assay, no system has been established to evaluate its transport activity in mammalian cells. In this study, we demonstrated that the exposure of cells expressing click beetle luciferase (bLuc) and SLC17A3 to D-luciferin produces marked bioluminescence, which enables the evaluation of SLC17A3 function.
View Article and Find Full Text PDFJ Cardiothorac Surg
January 2025
Department of General Internal Medicine, Hangzhou Xixi Hospital, Hangzhou Sixth People's Hospital, Hangzhou Xixi Hospital Affiliated to Zhejiang Chinese Medical University, Hangzhou, 310023, China.
Background: Gout is a metabolic disease caused by decreased blood uric acid excretion and purine metabolism disorders. Long-term and persistent metabolic dysfunction gradually affects other organ functions and is the main factor inducing Myocardial Infarction (MI) and Heart Failure (HF), seriously affecting the health of patients. This study adopts a meta-analysis to analyze the risk of MI and HF in gout patients.
View Article and Find Full Text PDFFood Chem
January 2025
Key Laboratory of Food Nutrition and Functional Food of Hainan Province, School of Food Science and Engineering, Hainan University, Haikou 570228, China. Electronic address:
Paederia scandens (Lour.) Merrill flavonoid-rich extract (PSMF) has shown excellent xanthine oxidase (XOD) inhibitory activity in our previous study. However, the efficacy of PSMF in mitigating hyperuricemia (HUA) remains to be elucidated.
View Article and Find Full Text PDFFASEB J
January 2025
Department of Internal Medicine, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, China.
Serum uric acid is an end-product of purine metabolism. Uric acid concentrations in excess of the physiological range may lead to diseases such as gout, cardiovascular disease, and kidney injury. The kidney includes a variety of cell types with specialized functions such as fluid and electrolyte homeostasis, detoxification, and endocrine functions.
View Article and Find Full Text PDFFoods
December 2024
Key Laboratory of Geriatric Nutrition and Health, Beijing Technology and Business University, Ministry of Education, Beijing 100048, China.
Hyperuricemia, a disorder of purine metabolism associated with cardiovascular disease, gout, and kidney disease, can be alleviated by food-derived peptides. However, the precise mechanisms remain unclear, hindering their development. This study reviews uric acid-lowering peptides from various sources, focusing on two pathways: inhibiting uric acid production and promoting excretion.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!