# Uric acid and hyperuricemia in relation to non-alcoholic fatty liver disease among individuals with type 2 diabetes: insights from a cross-sectional analysis

**Authors:** Chunbo Li, Mengfan Zhang, Mengchun Li, Qifeng Shao

PMC · DOI: 10.3389/fendo.2026.1720601 · Frontiers in Endocrinology · 2026-03-02

## TL;DR

This study finds that high uric acid levels and hyperuricemia are independently linked to non-alcoholic fatty liver disease in people with type 2 diabetes.

## Contribution

The study establishes a novel independent association between uric acid and NAFLD in T2DM patients using cross-sectional analysis and non-linear modeling.

## Key findings

- Hyperuricemia is independently associated with a 66% higher risk of NAFLD in T2DM patients.
- Each 1 μmol/L increase in uric acid raises NAFLD risk by 0.3%, and a standard deviation increase raises it by 26.6%.
- Uric acid levels show a linear relationship with NAFLD likelihood in T2DM patients, confirmed by RCS and GAM analyses.

## Abstract

Considering the growing evidence linking metabolic abnormalities with liver diseases, in adults with type 2 diabetes mellitus (T2DM), this research examined the relationship between serum uric acid (UA), hyperuricemia, and non-alcoholic fatty liver disease (NAFLD) in T2DM patients.

Between January 2024 and January 2025, 952 individuals with T2DM were enrolled in a single-center cross-sectional investigation conducted at the Zhengzhou People’s Hospital. Associations of UA and hyperuricemia with NAFLD were evaluated using multivariate logistic regression, accompanied by subgroup and sensitivity analyses. Restricted cubic spline (RCS) and generalized additive models (GAM) anlyses were applied to examine the non-linear dose–response association between UA and NAFLD.

Using the fully adjusted multivariate logistic regression model, hyperuricemia was found to be independently linked to a higher risk of NAFLD (OR 1.660, 95% CI: 1.094–2.521, p = 0.017). For serum UA, a rise of 1 μmol/L and a single standard deviation (SD) in its concentration corresponded to a 0.3% and 26.6% greater likelihood of developing NAFLD, respectively (OR 1.003, 95% CI: 1.001–1.005; OR 1.266, 95% CI: 1.050–1.526). Subgroup analyses revealed that hyperuricemia remained independently linked to NAFLD among individuals aged > 60 years, with hypertension, overweight/obesity, or without hyperlipidemia (p < 0.05). Furthermore, an elevation of one SD for UA levels was associated with a greater likelihood of NAFLD in several subgroups, including patients aged > 60 years, males, those without hyperlipidemia, and those with overweight/obesity (p < 0.05). Sensitivity analysis excluding patients with chronic kidney disease yielded consistent results: hyperuricemia remained significantly associated with NAFLD (OR 1.678, p = 0.032), and each 1-SD increase in UA was associated with a 31.6% increased risk (OR 1.316, p = 0.010). RCS analysis revealed a notable linear association for UA levels with the likelihood of NAFLD (p overall < 0.05, non-linearity p > 0.05). Similarly, GAM analysis further confirmed a statistically significant linear relationship between UA and NAFLD.

Serum UA levels and hyperuricemia are independently linked to a greater likelihood of NAFLD among individuals with T2DM, underscoring the importance of UA surveillance in this group to facilitate prompt detection and precise intervention for NAFLD.

## Linked entities

- **Diseases:** type 2 diabetes mellitus (MONDO:0005148), non-alcoholic fatty liver disease (MONDO:0013209), hyperuricemia (MONDO:0002144)

## Full-text entities

- **Diseases:** overweight (MESH:D050177), hyperlipidemia (MESH:D006949), metabolic abnormalities (MESH:D008659), hyperuricemia (MESH:D033461), chronic kidney disease (MESH:D051436), hypertension (MESH:D006973), liver diseases (MESH:D008107), T2DM (MESH:D003924), obesity (MESH:D009765), NAFLD (MESH:D065626)
- **Chemicals:** UA (MESH:D014527)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

44 references — full list in the complete paper: https://tomesphere.com/paper/PMC12989366/full.md

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Source: https://tomesphere.com/paper/PMC12989366