Dietary beer ameliorates glyoxylic acid-induced calcium oxalate nephrolithiasis in mice
4 affiliations
- 1School of Food Science and Engineering, Ningbo University , ,
- 2Department of Clinical Laboratory, Xiangshan Red Cross Taiwan Compatriot Hospital Medical and Health Group , , ,
- 3Department of Laboratory Medicine, The First Affiliated Hospital of Ningbo University , ,
- 4School of Laboratory Medicine and Life Science, Wenzhou Medical University , ,
Abstract
Introduction: Calcium oxalate (CaOx) nephrolithiasis is a major global health burden with limited non-pharmacological preventive options. Although moderate beer consumption has been linked to a lower risk of stone formation, the underlying mechanisms remain unclear. This study aimed to investigate the anti-lithogenic effects of dietary beer and the molecular pathways involved.
Methods: We combined a retrospective clinical analysis of 415 urolithiasis patients with a glyoxylic acid–induced mouse model. Male C57BL/6J mice received low-/high-dose beer (3/6 mL/kg) by gavage. We assessed renal histology, urinary biochemistry, oxidative stress, inflammatory responses, and the expression of crystal-adhesion molecules (CD44, OPN, Kim-1).
Results: In the clinical cohort, calcium oxalate monohydrate (COM) stones predominated (79.0%), with a male predominance (2.1:1). In mice, beer intervention lowered urinary oxalate and calcium concentrations, reduced histopathological injury and collagen deposition, downregulated CD44/OPN protein, decreased CD44/Kim-1/TNF-α/IL-1β mRNA expression, and partially preserved catalase and superoxide dismutase activities. The benefits were unlikely attributable to ethanol-induced diuresis, given the minimal gavage volume (~1.2–4% of fluid intake) and low ethanol delivery (~1.4–2.8 mg), which was further supported by unchanged daily water consumption.
Discussion: These findings demonstrate that dietary beer attenuates CaOx stone formation and modulates urinary, inflammatory, oxidative, and adhesion markers. The anti-lithogenic potential of beer constituents supports the development of purine-free, non-alcoholic, hops-derived polyphenol preparations as a testable hypothesis. However, the absence of appropriate controls precludes attributing the effects to any single component, and these results should not be interpreted as a clinical recommendation to consume beer.
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BibTeX
@article{yang2026dietary,
title = {{Dietary beer ameliorates glyoxylic acid-induced calcium oxalate nephrolithiasis in mice}},
author = {Yaoyao Yang and Xinyu Deng and Junge Zhang and Yanping Dai and Xueqian Wu and Wei Liang},
journal = {Frontiers in nutrition},
year = {2026},
month = oct,
doi = {10.3389/fnut.2026.1963460},
url = {https://europepmc.org/article/PMC/PMC13724572},
note = {CC BY},
}
RIS
TY - JOUR
TI - Dietary beer ameliorates glyoxylic acid-induced calcium oxalate nephrolithiasis in mice
AU - Yaoyao Yang
AU - Xinyu Deng
AU - Junge Zhang
AU - Yanping Dai
AU - Xueqian Wu
AU - Wei Liang
PY - 2026
DA - 2026/10/19
JO - Frontiers in nutrition
DO - 10.3389/fnut.2026.1963460
UR - https://europepmc.org/article/PMC/PMC13724572
AB - Introduction: Calcium oxalate (CaOx) nephrolithiasis is a major global health burden with limited non-pharmacological preventive options. Although moderate beer consumption has been linked to a lower risk of stone formation, the underlying mechanisms remain unclear. This study aimed to investigate the anti-lithogenic effects of dietary beer and the molecular pathways involved. Methods: We combined a retrospective clinical analysis of 415 urolithiasis patients with a glyoxylic acid–induced mouse model. Male C57BL/6J mice received low-/high-dose beer (3/6 mL/kg) by gavage. We assessed renal histology, urinary biochemistry, oxidative stress, inflammatory responses, and the expression of crystal-adhesion molecules (CD44, OPN, Kim-1). Results: In the clinical cohort, calcium oxalate monohydrate (COM) stones predominated (79.0%), with a male predominance (2.1:1). In mice, beer intervention lowered urinary oxalate and calcium concentrations, reduced histopathological injury and collagen deposition, downregulated CD44/OPN protein, decreased CD44/Kim-1/TNF-α/IL-1β mRNA expression, and partially preserved catalase and superoxide dismutase activities. The benefits were unlikely attributable to ethanol-induced diuresis, given the minimal gavage volume (~1.2–4% of fluid intake) and low ethanol delivery (~1.4–2.8 mg), which was further supported by unchanged daily water consumption. Discussion: These findings demonstrate that dietary beer attenuates CaOx stone formation and modulates urinary, inflammatory, oxidative, and adhesion markers. The anti-lithogenic potential of beer constituents supports the development of purine-free, non-alcoholic, hops-derived polyphenol preparations as a testable hypothesis. However, the absence of appropriate controls precludes attributing the effects to any single component, and these results should not be interpreted as a clinical recommendation to consume beer.
SN - 2296-861X
ER -