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Characteristics of serum bile acid profiles among individuals with metabolic dysfunction-associated steatotic liver disease

BMC Gastroenterology volume 25, Article number: 334 (2025) Cite this article

Abstract

Background

Metabolic dysfunction-associated steatotic liver disease (MASLD) has become the predominant chronic liver condition globally. Bile acid (BA) metabolism contributes significantly to MASLD progression. In this multicenter clinical study, we aimed to characterize serum BA profiles in patients with MASLD and identify specific alterations compared to healthy controls.

Methods

All MASLD cases were sourced from the gastroenterology outpatient departments of Shanghai Baoshan Hospital of Integrated Chinese and Western Medicine, Shanghai Baoshan District Songnan Community Health Service Center, and Lianyungang Oriental Hospital between June 2015 and December 2019. The data were analyzed using SPSS version 26.0, with a p-value of less than 0.05 considered significant.

Results

A total of 215 participants (35.3% women) with MASLD and 49 controls (44.9% women), aged 18–65 years, were included. MASLD patients showed higher levels of serum total BA (TBA), cholic acid (CA), chenodeoxycholic acid (CDCA), and ursodeoxycholic acid (UDCA) (p < 0.05, p < 0.01) when compared to controls. Furthermore, women patients with MASLD demonstrated notably higher levels of lithocholic acid (LCA), glycolithocholic acid (GLCA), and taurolithocholic acid (TLCA) than men patients with MASLD (p < 0.025, p < 0.01). Compared to women, men exhibited a higher proportion of primary to secondary BAs. Additionally, in men patients with MASLD, the serum concentrations of CA, CDCA, glycocholic acid (GCA), glycochenodeoxycholic acid (GCDCA), and taurochenodeoxycholic acid (TCDCA) exhibited significant negative correlations with ALT levels, while deoxycholic acid (DCA) and TLCA showed negative correlations with BMI.

Conclusions

Patients with MASLD exhibited notable variations in BA profiles, including sex-specific differences. This study provides corresponding evidence on the association between BAs and MASLD.

Trial registration

Chinese Clinical Trial Registry, NO: ChiCTR-OOC-15006157, registration date: March 25, 2015.

Peer Review reports

Introduction

Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as non-alcoholic fatty liver disease (NAFLD) [1], encompasses a broad spectrum of metabolic stress-related liver injuries, predominantly characterized by fat storage, inflammation, and in some cases, leading to necrosis of liver parenchymal cells [2]. Globally, the prevalence of MASLD stands at 30% [3], positioning it as the predominant cause of chronic liver conditions, with a marked escalation in its occurrence observed in recent times [4]. Currently, the US Food and Drug Administration has granted approval solely to resmetirom for the treatment of metabolic dysfunction-associated steatohepatitis (MASH). However, its efficacy does not fully meet the needs of the disease and new therapies need to be developed [5, 6].

Bile acids (BAs) are essential constituents of bile, synthesized by the liver and released into the biliary system. They undergo daily circulation between the liver and intestine via the portal vein [7]. BAs are pivotal signal transduction molecules in vivo, orchestrating metabolism through the farnesoid X receptor (FXR) and Takeda G protein-coupled receptor 5 (also known as GPBAR1). Impaired BA metabolism is correlated with MASLD onset and progression [8].

Although the pathogenesis of MASLD is not yet completely elucidated, it encompasses the accumulation of lipotoxic substances, hepatocyte injury, endoplasmic reticulum stress, and others [9]. An emerging collection of research implies that BA metabolism is probably a key factor in the development and advancement of MASLD [10]. With the disruption of the liver's normal architecture and functionality, there is an escalation in the production and release of BAs that deviate from the norm, consequently leading to changes in the BA spectrum that may induce liver toxicity. This, in turn, triggers the production of excessive toxic metabolites and cytokines, subsequently fostering MASLD genesis and progression [11]. Hence, BA metabolism has emerged as an appealing focus for the prevention and treatment of MASLD [12].

Studies have yielded conflicting results regarding alterations in the serum BA spectra of participants with MASLD, and little has been reported on the characterization of sex differences in BAs [7]. Therefore, this study aimed to characterize serum BA profiles in patients with MASLD and identify specific alterations compared to healthy controls.

Methods

Study design

This multicenter clinical study evaluated the BA profiles in healthy controls and patients with MASLD (No. ChiCTR-OOC- 15006157). This study utilized a non-randomized convenience sample, including 215 participants with MASLD and 49 healthy controls. All cases were sourced from the gastroenterology outpatient departments of Shanghai Baoshan Hospital of Integrated Chinese and Western Medicine, Shanghai Baoshan District Songnan Community Health Service Center, and Lianyungang Oriental Hospital between June 2015 and December 2019. A comprehensive set of anthropometric, medical, and lifestyle data from 264 participants was assessed, and blood samples were collected.

Ethics

The study design was approved by the Medical Ethics Committee of Baoshan District Hospital of Integrated Chinese and Western Medicine (No. 2014xbn01). All study participants provided written informed consent prior to enrollment.

Study population

This study included healthy controls and participants with MASLD aged 18–65 years. The diagnosis of MASLD followed the EASL-EASD-EASO Clinical Practice Guidelines on the management of MASLD: hepatic steatosis in conjunction with at least one cardiometabolic risk factor [13].

Patients who were pregnant or lactating were excluded, as well as those with severe cardiovascular diseases, neurological diseases, respiratory diseases, renal diseases, and other major diseases. Additionally, patients with other liver diseases, such as chronic viral hepatitis, human immunodeficiency virus infection, excessive alcohol consumption (> 30 g/day in men and > 20 g/day in women), drug-induced hepatic steatosis (including usage of systemic steroids) or a history of hepatocellular carcinoma, hepatic decompensation, liver resection, liver transplant were excluded. Detailed exclusion criteria are provided in the Supplementary Materials.

Sample processing

The patients were instructed to adhere to a light diet and refrain from smoking and drinking the day before sampling to minimize metabolic fluctuations [14]. After 8:00 p.m. the day before collection, the patients fasted, refrained from drinking water, and rested regularly. Fasting venous blood, amounting to 10 ml, was drawn from the participants in the morning, the samples were allowed to stand for 2 h at a temperature of 4 °C prior to centrifugation at a speed of 3000 revolutions per minute for a duration of 15 min. The collected supernatant was then stored at a temperature of − 80 °C for subsequent analysis of clinical biochemical markers.

Clinical chemistry

Alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transpeptidase (GGT), total bilirubin (TBIL), direct bilirubin, (DBIL), Triglyceride (TG), Total Cholesterol (TC), High-Density lipoprotein cholesterol (HDL-C), Low-Density Lipoprotein Cholesterol (LDL-C), albumin (ALB), fasting blood glucose (FBG), creatinine (CR), and levels of uric acid (UA) were assessed with an automated biochemical analyzer (Beckman Coulter Beckman, No. AU5800).

BA detection

Serum BA concentrations were quantified using ultra-high-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) (US SCIEX, Model API3200). The BAs measured included Cholic acid (CA), chenodeoxycholic acid (CDCA), deoxycholic acid (DCA), lithocholic acid (LCA), ursodeoxycholic acid (UDCA), glycocholic acid (GCA), glycochenodeoxycholic acid (GCDCA), glycodeoxycholic acid (GDCA), glycolithocholic acid (GLCA), glycodeoxycholic acid (GUDCA), taurocholic acid (TCA), taurochenodeoxycholic acid (TCDCA), taurodeoxycholic acid (TDCA), taurolithocholic acid (TLCA) and tauroursodeoxycholic acid (TUDCA) levels (detailed informations are in the Supplementary Materials).

Statistical analysis

All experimental data were analyzed using IBM SPSS Statistics for Windows, version 26.0 (International Business Machines Corporation, Armonk, New York, USA). The normality of the data distributions was tested using the Shapiro–Wilk test. Normally distributed data are expressed as means ± standard deviation, while non-normally distributed data are expressed as medians (interquartile range). A t-test was used for data conforming to a normal distribution, while the Mann–Whitney U test was used for data not conforming to a normal distribution. Pearson correlation analysis was used to assess relationships between normally distributed continuous variables, while Spearman correlation analysis was applied to non-normally distributed variables. Statistical significance was set at p < 0.05. Bonferroni correction for multiple testing was applied [15]. In some section, we compared the data for each of the two groups. Therefore, the significance level p = 0.05 was divided by two, which provides a significance level corrected for multiple testing: p = 0.025.

Results

Participant characteristics

Table 1 presents the demographic and baseline characteristics of the participants in the study. The analysis encompassed a total of 264 participants, including 215 participants diagnosed with MASLD and 49 controls. The control group was selected to approximate the MASLD group in age, sex, and geographic background. There were no significant differences in terms of age or sex between the groups with and without MASLD (p = 0.054 and p = 0.212). The levels of body mass index (BMI), ALT, TG, TC, and FBG were markedly elevated in the MASLD group compared to the healthy individuals (p = 0.008, p = 0.005, p = 0.005, p = 0.006, p < 0.001). Conversely, the HDL-C level was considerably lower in the MASLD group in comparison to the control group (p = 0.025).

Table 1 Demographic characteristics and serum chemistries of the study participants
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Serum BA profiles differ significantly in patients with MASLD

Concentrations of total BA (TBA) in serum were significantly elevated in the MASLD group relative to the control cohort (p < 0.01) (Fig. 1A). Specifically, serum levels of CA, CDCA, and UDCA were significantly elevated among individuals with MASLD (p < 0.05, p < 0.01) (Fig. 1B), although no significant variations were observed for other BAs, increasing trends were observed. In addition, the composition ratios of each BA also did not differ significantly (Fig. 1C).

Fig. 1
figure 1

Serum bile acid (BA) profiles in healthy controls (filled with lines, n = 49) and patients with metabolic dysfunction-associated steatotic liver disease (MASLD) (filled with color, n = 215). A Representative comparison of total bile acid (TBA) levels between healthy controls and patients; B Comparisons of 15 BAs between healthy controls and patients with MASLD. The TBA concentrations represent the sum of unconjugated, glycine- and taurine-conjugated BAs. Data are presented as mean (nM) and standard error of the mean. C Proportions of BAs in healthy controls and patients with MASLD. *P < 0.05 **P < 0.01 MASLD vs. healthy control

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No significant age-related differences in serum BA profiles were observed among patients with MASLD

To explore the influence of age on serum BA profiles in patients with MASLD, the MASLD group was stratified and compared according to median age. The findings indicated that there was no substantial variation in the composition of serum BA profiles between the MASLD group aged ≤ 51 years (n = 111) and > 51 years (n = 104) (Fig. 2A).

Fig. 2
figure 2

Comparison of serum bile acid (BA) profiles in healthy controls (filled with lines, n = 49) and patients with metabolic dysfunction-associated steatotic liver disease (MASLD) (filled with color, n = 215) stratified by age and sex. A Comparison of serum BA profiles in healthy controls and patients with MASLD aged ≤ 51 years (blue) and > 51 years (red). B Comparison of serum BA profiles between men (blue) and women (red) healthy controls and patients with MASLD. C Proportions of primary (gray) and secondary BAs (orange) in healthy controls and patients with MASLD. D Comparison of primary to secondary BAs between men and women healthy controls and patients with MASLD. E Proportions of conjugated (gray) and unconjugated BAs (orange) in healthy controls and patients with MASLD. F Comparison of conjugated to unconjugated BAs between men and women healthy controls and patients with MASLD. *P < 0.05 **P < 0.01 men vs. women

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Men and women patients with MASLD have more differential BAs compared with healthy controls

When patients with MASLD were stratified by sex, significant differences in serum BA profiles were detected between the men (n = 139) and women (n = 76) patients with MASLD. Specifically, women subjects with MASLD exhibited significantly higher levels of LCA, GLCA and TLCA compared to their men counterparts (p < 0.025, p < 0.01). While in healthy controls, significantly elevated level of GCDCA were observed exclusively in women individuals compared to men (p < 0.025) (Fig. 2B). Furthermore, men with MASLD had a higher proportion of primary to secondary BAs than women, which was absent in healthy controls (Fig. 2C, D). No significant differences were noted in the levels of conjugated and unconjugated BAs between the healthy controls and those with MASLD. (Fig. 2E, F).

BA profiles are correlated with ALT and BMI in men patients with MASLD

MASLD patients, regardless of sex, were stratified based on ALT levels, defined as normal (≤ 50 U/L for men and ≤ 40 U/L for women) and elevated (> 50 U/L for men and > 40 U/L for women) [16], as well as BMI, categorized as normal (< 24 kg/m2) and elevated (≥ 24 kg/m2) [17]. Differences in BA profiles were observed between men with MASLD who exhibited normal versus elevated ALT levels. In the patients with elevated ALT levels, there were significant decreases in serum concentrations of CDCA, GCA, GCDCA, and TCDCA (p < 0.025, p < 0.01) (Fig. 3A). However, no significant differences were observed in the serum BA profiles of women MASLD patients. Furthermore, a notable reduction in serum GCA and TLCA levels was observed in MASLD patients with an elevated BMI as opposed to those with a normal BMI (p < 0.05). After corrected using the Bonferroni method, no significant difference were identified when comparing the two groups (Fig. 3B). Spearman correlation analysis revealed that BA profiles in men patients with MASLD were correlated with ALT levels and BMI (Fig. 3C).

Fig. 3
figure 3

Comparison of serum bile acid (BA) profiles between men (blue) and women (red) patients stratified by alanine transaminase (ALT) level and body mass index (BMI). A Comparison of serum BA profiles between normal and high ALT groups in men and women MASLD patients (B) Comparison of serum BA profiles between normal and elevated BMI groups in men and women MASLD patients (C) Spearman correlation between plasma levels of individual BAs and ALT and BMI according to sex. *P < 0.05, **P < 0.01, ***P < 0.01

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Discussion

In this research, we explored the variations in the serum BA profiles among individuals with MASLD. Our observations indicated a markedly higher concentration of TBA in the serum of MASLD patients when contrasted with the healthy controls, particularly in CA, CDCA, and UDCA levels. Moreover, we observed differences in LCA, GLCA, and TLCA levels between women and men patients with MASLD. Furthermore, BA profiles demonstrated a significant inverse correlation with both ALT levels and BMI in men patients with MASLD, whereas no such association was observed in women patients.

In recent years, BAs have attracted significant attention as signaling molecules that regulate glycolipid metabolism [18]. The biosynthesis of BA is primarily mediated by two distinct pathways: the classical and alternative routes. The classical route, which begins with the action of cholesterol- 7α-hydroxylase (CYP7 A1), mainly produces CA and CDCA. In contrast, the alternative pathway, initiated by CYP27 A1, primarily synthesizes CDCA [19]. Based on their sources, BAs are categorized as primary or secondary. In humans, primary BAs such as CA and CDCA are conjugated with taurine or glycine in the liver to form bile salts. Subsequently, the gut microbiota transforms primary BAs into secondary BAs through sequential enzymatic reactions: bile salt hydrolase-mediated deconjugation, bile acid inducible operon-dependent 7α-dehydroxylation, and hydroxysteroid dehydrogenase-catalyzed epimerization, with each step critically shaping BA diversity and bioactivity [7, 20].

Alterations in serum BA profiles among individuals with MASLD are conspicuous and may be linked to changes in hepatic BA-related synthesis, transport genes, and intestinal microorganisms [21]. Our study initially observed a significant elevation of serum TBA in individuals with MASLD when contrasted to the healthy controls, a finding that aligns with prior research [22, 23]. Under physiological conditions, the BA pool remains stable because of the functioning transport system; however, in MASLD, the expression of rate-limiting enzymes involved in the classical pathway of BAs synthesis is markedly upregulated, leading to the conversion of cholesterol into BAs [7, 24], consequently resulting in increased serum TBA levels. Furthermore, our findings revealed a notably elevated concentration of CA, CDCA, and UDCA in the serum BA profile of MASLD patients. Previous studies highlighted similar findings, such as Nimer et al., who analyzed serum BA profiles of 102 Americans diagnosed with MASLD by biopsy and noted a significant rise in serum CDCA in these patients [23]. Ferslew demonstrated significantly higher serum CDCA and UDCA in individuals with non-alcoholic steatohepatitis compared to the healthy population, while CA showed an increasing trend [25]. Similarly, Caussy observed significantly increased serum CA and CDCA combinations in patients with MASLD [26]. In their BA profiles analysis on stool samples from 28 Canadian patients diagnosed with MASLD by biopsy, Mouzaki et al., reported significant increases in fecal CA and CDCA levels, along with a rising trend in UDCA levels [27]. Our results and those of other studies highlight consistent significant increases in CDCA levels. CDCA, as the primary BA and the most potent FXR agonist among BAs [28], may overstimulate FXR-mediated signaling in the gut and is also a potent inducer of epithelial permeability [29]. This increased CDCA level may lead to the breakdown of the intestinal epithelial barrier and ultimately contribute to MASLD progression. Furthermore, differences in BAs between healthy controls and patients with MASLD observed in other studies were likely related to factors such as diagnostic criteria (liver biopsy), baseline levels of the included population, BMI, sex ratio, and ethnic differences.

Current research suggests that elevated BA levels are both a cause and a consequence of MASLD [7]. In other words, MASLD and BA dysregulation form a bidirectional process: hepatic steatosis disrupts BA synthesis and secretion, while BA abnormalities can further promote lipid accumulation and inflammation, driving disease progression. From a therapeutic perspective, modulating BA metabolism remains a promising strategy. For example, Obeticholic acid (OCA), a BA analogs, has shown some efficacy in clinical trials of MASH, including improvements in fibrosis [30]. However, due to side effects such as pruritus, it was not approved by the FDA for MASH treatment [31]. Nevertheless, OCA’s trial results demonstrated the therapeutic potential of targeting BA receptors in MASLD. Recent studies have identified other BAs with therapeutic potential. For example, 3-succinylated cholic acid [32] and hyodeoxycholic acid [33] have shown promise in MASLD. These BAs may offer safer and more effective interventions for MASLD in the future. Targeting BA signaling pathways remains an important area for further research [34].

Sex differences in the manifestation of metabolic diseases have been documented [35, 36]. Balakrishnan et al., in their meta-analytic review, found that the prevalence of MASLD was 19% less in women than in men [37]. Our research examined the sex-associated variations in serum BA patterns among individuals with MASLD. Women exhibited considerably elevated levels of LCA, GLCA, and TLCA compared to men, whereas in healthy controls, elevated levels of GCDCA were exclusively observed in women compared to men, suggesting the presence of differences in serum BA profiles between sexes, which may be amplified by MASLD [38]. As mentioned above, BA profiles are affected by the gut microbiota, which is regulated by sex hormones [39], thus, sex hormones may affect BA profiles by affecting the gut microbiota. Studies have confirmed sex-specific differences in BA profiles [39, 40], with women mice frequently exhibiting higher BA synthesis rates and BA pool sizes than men mice [41]. OrgE reported significantly different hormone status between male mice fed normal and high-fat diets, which affected the composition of the microbiome, which was more common in women mice fed high-fat diets. Hormonal changes strongly affect BA profiles, and sex-specific differences in BA profiles are more prominent in high-fat and high-sugar diets [42]. These findings are consistent with our clinical observations. We observed a higher ratio of primary to secondary BAs in men with MASLD than in women. Nonetheless, it remains to be determined whether this observation is directly responsible for the disparities in BAs levels between MASLD-afflicted men and women and their healthy counterparts. Considering the important role of gut microorganisms in the conversion of primary BAs to secondary BAs, future studies should perform microbiological analyses of feces or tissues from patients with MASLD to elucidate whether the microbiome explains the differences in BA profiles between men and women [43, 44].

Elevated serum liver enzymes and obesity are linked to a higher likelihood of developing MASLD [45]. In our study, men with MASLD who had elevated ALT levels exhibited significantly lower BA levels compared to those with normal ALT levels. This finding may be explained by two possible mechanisms. First, inflammatory cytokines in hepatic inflammation may suppress BA synthesis. Elevated ALT reflects hepatocellular injury and inflammation, where pro-inflammatory cytokines downregulate CYP7 A1, reducing BA production as a protective response [46]. Second, sex-specific differences in BA metabolism may play a role. Male patients may more effectively regulate BA composition and excretion, potentially due to androgen-induced BA clearance, differences in conjugation patterns, and gut microbiota variations [47]. These adaptations might buffer BA dysregulation during hepatic inflammation, preventing excessive accumulation. However, further research is needed to elucidate the precise role of these factors in MASLD progression.

Our analysis of patients with MASLD according to sex revealed that in men patients, the serum levels of CA, CDCA, GCA, GCDCA, and TCDCA exhibited mostly negative correlations with ALT levels, while DCA and TLCA showed negative correlations with BMI. This contrasts with reports by Nimer et al., who observed positive correlations between CA, GCA, GCDCA and TCDCA with ALT in patients with MASLD, while reporting no significant correlation with BMI [48]. This discrepancy could be attributed to differences in sex grouping, diagnostic criteria, and baseline population levels, including higher BMI, sex ratios, and ethnic disparities in previous studies. These factors warrant attention in future studies to provide further insight.

This study has several limitations. First, the cross-sectional design does not allow for the determination of causality. Future longitudinal studies are required to elucidate the temporal dynamics and potential causative pathways underlying these associations. Second, the use of a non-randomized convenience sample may introduce selection bias and limit the generalizability of the findings. Third, the unequal sample sizes between the MASLD group and the control group may introduce bias, complicate the interpretation of the findings, and may limit the statistical power required to detect significant correlations or differences. Additionally, the study did not include microbiome analyses, which limits our ability to interpret gut-liver axis influences on BA profiles.

Conclusions

Our findings demonstrate notable variations in BA profiles with sex-specific differences in patients with MASLD. An in-depth understanding of these BA spectrum characteristics in MASLD requires careful consideration of sex differences when studying the pathophysiological changes caused by MASLD. This study provides corresponding evidence on the association between BAs and MASLD.

Data availability

All data generated or analyzed during this study are included in this article. Further enquiries can be directed to the corresponding author.

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Acknowledgements

We thank the gastroenterology outpatient departments of Shanghai Baoshan Hospital of Integrated Chinese and Western Medicine, Shanghai Baoshan District Songnan Community Health Service Center, and Lianyungang Oriental Hospital for helping us collect data.

Funding

This study was supported by Clinical Research Plan of the Shanghai hospital development center (No. SHDC2020 CR4051 to QF), the National Natural Science Foundation of China (No. 82174186 to YH), the excellent doctoral projects in key fields of Shanghai University of Traditional Chinese Medicine (No. GJ2023016 to SL).

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Author notes

  1. Sheng Lyu and Jiani Yang contributed equally to this work.

Authors and Affiliations

  1. Institute of Liver Diseases, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China

    Sheng Lyu, Jiani Yang, Xin Xin, Qinmei Sun, Beiyu Cai, Xin Wang, Ziming An, Yiyang Hu & Qin Feng

  2. Central Laboratory, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China

    Qin Feng

  3. Key Laboratory of Liver and Kidney Diseases, Shanghai University of Traditional Chinese Medicine, Ministry of Education, Shanghai, China

    Xin Xin, Yiyang Hu & Qin Feng

  4. Clinical Laboratory, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China

    Jian Sun & Lei Shi

  5. Shanghai Qingpu Traditional Chinese Medicine Hospital, Shanghai, China

    Jiani Yang

  6. Baoshan District Hospital of Integrated Traditional Chinese and Western Medicine of Shanghai, Shanghai, China

    Xiaojun Gou

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  1. Sheng Lyu
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Contributions

All authors contributed to the conceptualization and design of the study. Sheng Lyu and Jiani Yang contributed equally to this work. JY and SL participated in the patient visits, data collection, analysis and interpretation of data, drafting of the manuscript. XX, QS, BC, XW, ZA participated in the patient visits, data collection. JS and LS participated in the detection and verification of sample. XG participated in the study concept and design, critical revision of the manuscript. YH provided valuable suggestions and funding support. QF participated in the study concept and design, critical revision of the manuscript, obtained funding, study supervision.

Corresponding authors

Correspondence to Lei Shi, Qin Feng or Xiaojun Gou.

Ethics declarations

Ethics approval and consent to participate

The study design was approved by the Medical Ethics Committee of Baoshan District Hospital of Integrated Chinese and Western Medicine in January 2014 (No. 2014xbn01). All study participants provided written informed consent prior to enrollment, and the study adhered to the ethical principles of the Declaration of Helsinki.

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Not applicable.

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The authors declare no competing interests.

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Lyu, S., Yang, J., Xin, X. et al. Characteristics of serum bile acid profiles among individuals with metabolic dysfunction-associated steatotic liver disease. BMC Gastroenterol 25, 334 (2025). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s12876-025-03903-1

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Keywords

BMC Gastroenterology

ISSN: 1471-230X

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