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Serum lipopolysaccharide binding protein (LBP) and metabolic syndrome: a systematic review and meta-analysis

Diabetology & Metabolic Syndrome volume 17, Article number: 268 (2025) Cite this article

Abstract

Background

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Studies reported a link between the inflammatory background of metabolic syndrome (MetS) and endotoxemia. Assessing endotoxemia is typically done by measuring lipopolysaccharides binding protein (LBP). Here, we aimed to find the exact efficacy of LBP in discriminating MetS cases from healthy individuals.

Methods

A systematic literature review was performed in Embase, Web of Science, Scopus, PubMed, and Google Scholar up to the end of April 2024. We included all original studies that provided data comparing the serum LBP levels between MetS and non-MetS populations or the association between LBP concentration and MetS. The National Institute of Health (NIH) checklist was utilized to assess the quality of included studies.

Main findings

Among 1930 records found in the initial search, 18 studies were included in the systematic review and 13 in the meta-analysis. All included reports had acceptable quality. Our findings showed significantly higher LBP levels among MetS compared to non-MetS individuals (SMD: 5.313 µg/ mL, 95% CI: 0.606 to 10.020, I2 = 99.681). To address this high heterogeneity, subgroup analysis, and sensitivity analysis were performed. Additionally, most of the included items in this investigation showed that higher serum LBP levels significantly increased the risk of MetS. Based on the Egger test, a considerable publication bias was observed.

Conclusion

Our findings suggest a potential association between higher levels of LBP and MetS, with MetS cases exhibiting elevated LBP levels compared to non-MetS participants. However, due to the high heterogeneity observed across studies, the influence of individual studies on the overall results, and the possibility of publication bias, these findings should be interpreted with caution.

Introduction

Metabolic syndrome (MetS) has spread all around the world in recent years due to the considerable changes in dietary habits and lifestyle [1]. Recently, MetS has attracted increased attention because of its close link with a cluster of medical issues such as nonalcoholic fatty liver disease (NAFLD), cardiovascular disease (CVD), and diabetes mellitus (DM) [2, 3]. MetS is typically defined as the presence of hypertriglyceridemia, hypertension, abdominal obesity, high blood sugar levels, and reduced serum high-density lipoprotein cholesterol (HDL-C) [4]. The prevalence of MetS in general adult populations ranged from 12 to 31% depending on the diagnostic criteria [5].

Every element of MetS can be a potential cardiovascular risk factor. Therefore, approximately half of the MetS cases suffer from atherosclerosis, heart failure, and myocardial infarction and their mortality rate is two times more than the general population [6,7,8]. On the other hand, the core concept of this condition is based on insulin resistance which has a pivotal role in DM development [9, 10]. Thus, to prevent these complications, having new approaches for early diagnosis is crucial, necessitating a comprehensive understanding of the pathophysiology of MetS. Though not fully elucidated, numerous studies agree that low-grade chronic inflammation is one of the key etiologies [11, 12].

Studies demonstrated higher levels of inflammatory markers such as Interleukin 6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor α (TNF-α) in MetS cases compared to normal individuals [13,14,15]. One of the possible causes of chronic inflammatory state among MetS cases might be due to endotoxemia, defined as the presence of endotoxin in blood. Endotoxins, which are lipopolysaccharides (LPS) found mainly in the outer membrane of gram-negative microbiomes, can enter the bloodstream either through systemic infection caused by exogen bacteria or via the gut microbiomes passing through the epithelium using chylomicrons [16, 17]. Emerging evidence suggests that this process is strongly influenced by gut microbiota dysbiosis, which increases intestinal permeability and facilitates LPS translocation into circulation. This condition, known as metabolic endotoxemia, triggers low-grade chronic inflammation—a key feature of MetS pathogenesis [18, 19]. Assessing endotoxemia is typically done by measuring LPS binding protein (LBP), an acute phase reactant protein that facilitates the interaction between LPS and toll-like receptor 4 (TLR4) and the cluster of differentiation 14 (CD14), owing to its long half-life [20]. LBP thus serves as a surrogate marker of host exposure to gut-derived endotoxins and may reflect the degree of inflammation and metabolic dysregulation in MetS [21]. This inflammatory response, when chronically activated, can interfere with insulin signaling pathways through several mechanisms, including the activation of c-Jun N-terminal kinase (JNK) and IκB kinase (IKK), which phosphorylate insulin receptor substrate-1 (IRS-1) at serine residues, thereby inhibiting its function in the insulin signaling cascade. Additionally, LPS-induced inflammation promotes the recruitment of macrophages to adipose tissue, further exacerbating local and systemic inflammation and contributing to insulin resistance [22]. Furthermore, different features of MetS such as dyslipidemia could accelerate this process by affecting jejunum motility and food passing time and causing gut microbiome leakage and endotoxemia [23].

To date, studies have reported inconsistent findings regarding the differences in LBP levels among individuals with and without MetS. While some investigations found no significant difference [24,25,26], others reported significantly higher levels of LBP among MetS. These discrepancies may stem from variations in study populations, methodologies, and the presence of underlying conditions. For instance different study population such as hemodialysis patients [27], human immunodeficiency virus (HIV) infected individuals [24], psoriatic patients [28], and type 1 DM cases [26] have been investigated. In this regard, we aimed to conduct a comprehensive review to find the exact efficacy of LBP in discriminating MetS cases from non-MetS individuals. We hypothesize that serum LBP levels are higher in individuals with MetS compared to non-MetS controls and that LBP is a potential biomarker for MetS risk assessment.

Methods

The protocol for this review was developed based on the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guidelines [29] and registered on the international Prospective Register of Systematic Reviews (PROSPERO) with the “CRD42024529880” registration number.

Search strategy

A systematic literature search was done through Medline (PubMed), Embase, Web of Science, and Scopus up to the end of April 2024 using various combinations of keywords and free-text terms related to Metabolic Syndrome (“Metabolic Syndrome” OR “MetS” OR “Metabolism Syndrome”) and Lipopolysaccharide-Binding Protein (“lipopolysaccharide-binding protein” OR “LBP” OR “LPS-binding protein” OR “lipopolysaccharide binding” OR Endotox* OR “Endotoxemia”). No language, date, or publication status restrictions were applied. Furthermore, the reference lists of the retrieved articles and the relevant reviews were examined to find eligible research. A manual search was conducted by screening the first 10 pages of Google Scholar results using the primary keywords “Metabolic Syndrome” and “Lipopolysaccharide-Binding Protein” to identify any potentially missed articles. We attempted to contact the correspondence in the case of unavailable full text. Details of the search string for each database are included in Supplementary File 1. After retrieving the search results and excluding duplicates, two researchers (SH-H and MM) separately screened the titles, abstracts, and full texts according to the prespecified criteria. Any disagreements were resolved through discussion, and if consensus could not be reached, a third reviewer (S.M-T) was consulted to make the final decision. The study selection process was done using the Rayyan platform [30].

Study selection

We included all original studies providing data on the comparison of serum LBP levels between MetS and non-MetS populations or the association between LBP concentration and MetS. Studies with no control group, in vitro studies, animal investigations, conference abstracts, and studies in languages other than English were excluded.

Data extraction

The data extraction process was conducted independently by two reviewers (SM-T and RA-B), and their results were compared. Any disagreements were resolved through discussion, and if consensus could not be reached, a third reviewer (M.H-B) was consulted to make the final decision. The extracted information from each included article was as follows: first author’s name, year of publication, study design, country of origin, characteristics of enrolled participants, number of participants (both MetS and Non-MetS groups), criteria for MetS diagnosis, the method for LBP measurement, the serum levels of LBP (mean ± standard deviation) in MetS and control participants, and the main outcome of the survey.

Quality assessment

The critical appraisal was performed independently by 2 authors (SH-H and MM) using the National Institution of Health (NIH) Quality Assessment Tool [31]. In case of any disagreement, consensus was reached through consultation with a third reviewer (MH-B). According to this scale, there are 14 items for cross-sectional, cohort, and controlled intervention studies and 12 items for case-control studies. Finally, based on the consensus among reviewers, each article is classified as good, fair, or poor quality.

Statistical analysis

After extracting the eligible data of the included studies, a meta-analysis was performed. The desired effect sizes were weighted mean difference (WMD) and 95% confidence intervals (CI) of serum LBP levels of both MetS cases and non-MetS ones. All statistical analysis was conducted using CMA version 3 software and a 2-sided 0.05 level of significance was used in all cases. The statistical heterogeneity between the results was determined using the inconsistency index (I2). According to the Cochrane collaboration tool [32], I2 below 40% might not be important, 30–60% indicate moderate heterogeneity, 50–90% represent substantial heterogeneity, and 75–100% show considerable heterogeneity. In the case of moderate to considerable heterogeneity, the random effect model was applied, otherwise the fixed effect model was utilized. The potential sources of this heterogeneity may also include differences in participant characteristics (e.g., age, sex), laboratory methods, and unmeasured confounding variables across studies, in addition to study design, geographic region, and diagnostic criteria for MetS. The pooled WMDs along with 95% CI were presented using forest plots. The leave-one-out method was utilized for sensitivity analysis. The possible publication bias was evaluated using the Egger emission bias assessment test. The subgroup analysis was conducted according to the study design, year of publication, and geographical region.

Results

Study selection process

The primary search in the mentioned databases yielded 1930 potentially relevant studies. Of which 976 were removed due to duplication. Thus, 954 records were gone for screening through the title and abstract. After screening 43 articles were eligible for further investigation through full text. Finally, 18 research were included in the systematic review and 13 in the quantitative analysis. The Kappa statistic for the screening process was 0.71, indicating an acceptable level of agreement between the reviewers. The detailed selection process is shown in Fig. 1.

Fig. 1
figure 1

PRISMA flow diagram

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Study characteristics

Table 1 outlines the included studies in the systematic review. These articles were published between 2010 and 2024, consisting of seven cross-sectional studies and three clinical trials; four other articles had a cohort study design, and finally, four studies were in a case-control manner. Overall, seven studies were carried out in Asia, seven in Europe, and the other four, in North America. Twelve studies investigated individuals with MetS as the only comorbidity. Some others have involved participants who had other conditions besides MetS, including outpatient hemodialysis cases [27], childhood acute lymphoblastic leukemia (cALL) survivors [33], psoriatic patients [28], HIV-infected individuals [24], diabetic cases [26] and old age patients with high CVD risk [34]. MetS was defined according to the National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP-III) in seven studies [24, 25, 27, 34,35,36,37,38]. Others have used the criteria of the International Diabetes Federation (IDF) [26, 28, 33, 39,40,41], NCEP-ATP-III for Asian-Americans [21], and the Japanese Society of Internal Medicine (Japanese criteria) [42]. Approximately, all included studies (except 2 studies [35, 43]) have utilized commercially available enzyme-linked immunosorbent assay (ELISA) method for measurement. Of the 18 included citations, 14 reports compared the mean and standard deviation (SD) for serum LBP levels between MetS and non-MetS participants. Four studies have evaluated the association between serum LBP levels and MetS prevalence. Using the NIH quality assessment tool, nine studies were qualified as good [21, 24, 25, 35,36,37,38,39, 42], and nine as fair [26,27,28, 33, 34, 41, 43,44,45] (Supplementary file 2).

Table 1 Characteristics of included studies
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Meta-analysis of mean difference of serum LBP levels between MetS and non-MetS

Of 14 studies reporting the desirable effect sizes, one study was excluded due to insufficient data [25]. These 13 studies include 700 MetS cases and 983 non-MetS individuals. According to the random effects model, the pooled mean difference of serum LBP demonstrated a significantly higher level among MetS compared to non-MetS participants (SMD: 5.313, 95% CI: 0.606 to 10.020, I2 = 99.681) (Fig. 2). Results of sensitivity analysis revealed no considerable change between the before-after sensitivity pooled SMD for all included studies except one report (Fig. 3). After removing Krishnan et al. [43], the pooled effect sizes were insignificant (SMD: 4.749, 95% CI: -0.089 to 9.587). Results of the Egger test demonstrated a considerable publication bias (Fig. 4).

Fig. 2
figure 2

Pooled effect sizes of all included studies in the meta-analysis

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Fig. 3
figure 3

Sensitivity analysis based on the leave-one-out method

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Fig. 4
figure 4

Funnel plot for publication bias of included studies

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The subgroup analysis was performed based on the study design, geographical region, MetS criteria, and publication year (Table 2). The pooled mean difference in case-control studies was in line with the overall result (SMD: 15.516, 95% CI: 11.004 to 20.029, I2 = 99.538). However, subgroup analysis among cross-sectional studies (SMD: 1.568, 95% CI: -1.544 to 4.680, I2 = 64.290) and RCTs (SMD: 3.152, 95% CI: -1.436 to 7.740, I2 = 67.805) demonstrated no significant differences in LBP levels between MetS and non-MetS. According to the geographical region, studies were categorized into Asia, Europe, and North America. Pooled effect sizes of studies in Asia showed higher serum LBP levels in MetS versus non-MetS (SMD: 10.599, 95%CI: 0.683 to 20.514, I2 = 99.918). However, a meta-analysis of studies in Europe (SMD: 1.738, 95% CI: -5.821 to 9.297, I2 = 49.129, p = 0.06) and North America (SMD: 6.302, 95% CI: -3.976 to 16.581, I2 = 48.037, p = 0.12) indicated no significant difference. Most included studies in the meta-analysis have utilized IDF or NCEP-ATP-III criteria for defining MetS. The pooled effect size of studies using NCEP-ATP-III criteria was marginally insignificant (SMD: 5.978, 95% CI: -0.616 to 12.573, I2 = 99.813, p = 0.07). Furthermore, the meta-analysis of investigations utilizing IDF criteria showed no significant difference (SMD: 2.778, 95% CI: -7.086 to 12.642, I2 = 41.099, p = 0.58). Besides, studies were also categorized into two groups based on the publication year. Pooled effect sizes of the studies published between 2012 and 2018 suggested no significant differences in LBP levels between MetS and non-MetS (SMD: 3.752, 95% CI: -2.845 to 10.349, I2 = 72.865). On the other hand, investigations between 2019 and 2024 showed higher serum LBP levels in MetS (SMD: 7.03, 95% CI: 0.12 to 13.94, I2 = 99.839). Some included studies involved participants with various comorbidities including elderly people at high cardiovascular risk [34], type 1 DM patients [26], hemodialysis patients [27], psoriatic patients [28], and HIV-infected individuals [24]. To assess whether these participants’ past medical histories could affect the results, a meta-analysis was conducted after excluding these publications. The pooled effect size demonstrated significantly higher LBP levels among MetS cases, but the heterogeneity remained high (SMD: 6.86, 95% CI: 0.46 to 13.26, I² = 99.786). Forest plots of the subgroup analysis were summarized in supplementary file 3.

Table 2 Subgroup analysis
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Association between serum LBP levels and MetS

Four studies evaluated the association between serum LBP levels and MetS. During a six-year follow-up, Liu et al. [21] demonstrated that higher LBP levels increased the possibility of MetS incidence among normal-weight participants, but not overweight and obese individuals. Sun et al. [36] showed that participants with higher LBP levels had higher odds of MetS prevalence. Another prospective investigation among the Japanese population suggested that higher LBP levels were associated with an increased risk of developing MetS during a five-year follow-up [42]. However, a survey among survivors of cALL found a marginally insignificant association between serum LBP levels and MetS incidence [33].

Discussion

As investigated in the literature, chronic LPS exposure leads to systemic insulin resistance and chronic low-grade inflammation, both of which are the main characteristics of MetS [34, 45]. LBP is considered as a marker for endotoxin exposure since its half-life (24 h) exceeds that of LPS (up to 3 h). Therefore, it has been a useful indicator of prolonged exposure to endotoxins [33]. However, the controversy on the association between endotoxemia markers and MetS has remained unconcluded. Results of the current meta-analysis indicate a significantly higher level of LBP among MetS vs. non-MetS participants. Besides, most of the included studies in the systematic review demonstrated that higher serum LBP concentrations significantly increased the risk of MetS [21, 36, 42]. Only one investigation among survivors of cALL showed a marginally insignificant association, which might be due to its specific population [33].

This significant relationship between serum LBP concentrations and the MetS has been explained through several mechanisms. As an acute-phase reactant that is produced mainly by the liver, LBP forms a complex with LPS in the bloodstream, presents LPS to CD14, and initiates a signaling cascade of inflammatory cytokines by interacting with TLR4 [39, 42]. Moreover, these cytokines, especially IL-6 and IL-1, stimulate the liver formation of acute-phase reactants and cause a vicious circle [35]. This systemic chronic inflammation can aggravate insulin resistance and impose a series of metabolic complications, such as dyslipidemia, glucose intolerance, and increased renal sodium reabsorption, causing increased blood pressure [46, 47]. On the other hand, abdominal adipose tissue has been introduced as a vital source of LBP secretion in patients with MetS, causing chronic low-grade inflammation [34, 41].

As mentioned before, different items including obesity, dyslipidemia, hypertension, and impaired glucose metabolism are needed for MetS diagnosis [48]. In this review, we only included the reports surrounding MetS itself, not its parameters. Some of the included reports have also assessed the relationship between metabolic profile and LBP levels. Five studies have suggested a positive correlation between waist circumference and serum LBP levels (Spearman’s correlation ranging from 0.12 to 0.48) [21, 34,35,36, 38]. This finding is in line with the results of Trøseid et al. [49], which demonstrated that LPS levels are closely correlated with the amount of intraabdominal fat. Moreover, Rexrode et al. [50] demonstrated that the composition and size of abdominal adipose tissue correlate with the amount of pro-inflammatory cytokines. This could be an explanation for why several hormonal and metabolic disturbances of MetS are pronounced in line with central obesity [34]. Four studies have shown that low HDL-C levels are associated with higher serum LBP levels [27, 33, 35, 36]. This could be explained by the pivotal role of HDL-C in regulating the inflammatory response. Having the highest binding capacity for LPS among all serum lipoproteins, HDL scavenges LPS, neutralizes it, and reduces the production of proinflammatory cytokines triggered by LPS [51]. Regarding the association between blood pressure and serum LBP levels, inconsistent results have been reported. Some included studies demonstrated a significant positive association [36, 42]. However, such association was not observed in other included studies [27, 33, 35, 39]. This might be because of upregulation in cytokines expression via TLR4, results in attenuation of smooth muscle contractility [52]. Based on the included reports, results surrounding the association between glucose metabolism and serum LBP levels are inconsistent. Some studies found significant positive association between fasting blood sugar (FBS) with LBP levels [27, 36], while other found no significant relation. According to the results of an in vivo investigation, LBP might play a role in the link between gut microbiota and glucose metabolism. They suggested that knockdown of LBP in liver improved the systemic glucose metabolism [53]. A systematic review on available literature up to October 2016 showed that elevated LPS levels could be a crucial factor in glucose metabolism and even complications of diabetes [54]. On the other hand, results of a five-year follow up study suggested that LBP alone cannot predict T2DM [55]. Thus, further longitudinal investigations are needed to better understand this association.

Endotoxemia is a common feature in chronic kidney disease (CKD) patients, especially those undergoing hemodialysis (HD) [56, 57]. Lim et al. [27] demonstrated that serum LBP level was significantly higher not only in HD patients with MetS compared to non-MetS but also in non-MetS HD cases compared to normal people. Thus, it seems essential to pay attention to gut microbiota composition in these populations.

As reviewed elsewhere, the presence of LPS in tobacco smoke can be a possible source of inflammation in smokers [58, 59]. In line with that, elevated levels of LBP were observed in the bronchoalveolar lavage fluid of smokers [60]. However, most of the included studies had either excluded smokers or did not report related data. In this regard, three studies [21, 25, 35] investigated this association, and only Gonzalez-Quintela et al. [35] demonstrated a significant correlation between smoking and LBP concentrations. This controversy might be due to the history of smoking and fluctuating levels of endotoxins in the blood. Further longitudinal studies are needed to better clarify this association. According to the available literature, alcohol consumption was found to increase intestinal permeability and as a result increased levels of endotoxin [61, 62]. Serum LBP levels were found to be higher among alcoholics than the general population [63]. A growing body of evidence suggested a close association between endotoxemia and alcoholic liver disease [64]. Two included studies have assessed this association and reported no significant relationship [21, 35].

As mentioned before, LBP is an acute-phase reactant protein that is synthesized in the liver, and its levels increase immediately after bacteremia or endotoxemia. LBP forms a complex with LPS and enhances its binding to CD14 receptors. This mechanism triggers a cascade of inflammatory molecules [35]. LPS could lead to hepatocyte injury by promoting the expression of TNF and activation of the mentioned inflammatory processes in Kupffer cells [65]. Of note, inhibition of endotoxin receptors in multiple animal models demonstrated considerable protection against the onset of NAFLD [66]. On the other hand, due to the close association of NAFLD with dyslipidemia, obesity, hypertension, and insulin resistance, it is commonly considered the hepatic manifestation of MetS [67, 68]. The presence of MetS in patients with NAFLD has been linked to an increased risk of developing non-alcoholic steatohepatitis (NASH), fibrosis, and even liver failure in the future [68]. Among the included studies, Gonzalez et al. [35] showed a correlation between serum levels of liver enzymes, particularly gamma-glutamyl transferase (GGT), and LBP concentrations. This correlation was found to be stronger among obese participants. This was in line with the findings of Sun et al. [36] In contrast, Liu et al. [21] results showed no correlation between LBP levels and GGT after adjusting for sex, age, religion, and residence.

According to the results of subgroup analysis, studies in a case-control manner suggested a significant difference in LBP concentrations between MetS and non-MetS. However, the pooled effect size of cross-sectional studies demonstrated no significant difference. That might be due to the nature of LBP which fluctuates in the blood. Therefore, it seems that the results of longitudinal investigations are more reliable. Another subgroup analysis based on region indicated a significant difference in the pooled effect size in Asia, while the findings from Europe and North America did not show significant differences. This may be due to various factors, such as differences in dietary habits, genetic predisposition, environmental influences, and even variability in the study designs across different regions [69].

The sensitivity analysis revealed that the Krishnan et al. [43] study had a substantial impact on the pooled effect size. When this study was removed, the pooled effect became marginally insignificant. This may be attributed to the notably high difference in mean serum LBP levels between MetS and non-MetS in their study. Moreover, They have employed an electrochemiluminescent assay to measure LBP levels, a method that differs from the ELISA technique used in the other studies included in the analysis. These methodological differences could have contributed to the study’s disproportionate influence on the overall results.

Dietary habit alterations, especially a high-fat diet, are associated with increased serum LPS levels through gut dysbiosis. Besides these dietary changes alter the intestinal barrier allowing an increase in permeability and translocation of LPS to the bloodstream [70]. Therefore, diet-based interventions targeting gut microbiota might be effective in reducing circulatory endotoxin. Investigations have demonstrated that consumption of fresh vegetables, fruits, and fish reduced systemic endotoxemia [71]. Probiotics and prebiotics are microbiota-management tools that found to be effective in reducing metabolic endotoxemia [72, 73]. However, there are conflicting results surrounding the efficacy of probiotic foods and supplements in the management of MetS [74]. Fecal microbiota transplantation (FMT) is another new therapeutic option. Studies demonstrated promising results of FMT in modulating MetS components [75]. Further studies are needed to better understand the efficacy of these interventions.

Strengths and limitations

To the best of our knowledge, this is the first systematic review and meta-analysis assessing the link between serum LBP and MetS. We included all observational and interventional investigations without any restriction on publication date, race, gender, and past medical history. However, this study has some limitations. First, heterogeneity exists in the pooled effect size of our study; therefore, the results should be interpreted cautiously. However, this heterogeneity was somewhat addressed through subgroup analysis. The significant heterogeneity may be attributed to variations in study design, country of origin, and the past medical history of participants. Approximately, all included studies used commercially available ELISA kits to measure LBP, with the method of assessment being consistent across studies. However, the specific brands of the kits varied, which could contribute to some degree of heterogeneity in the results. Other factors, such as age and smoking status, also appeared to influence serum LBP levels, which could further explain the observed heterogeneity [35]. Unfortunately, due to limited data, we were unable to conduct subgroup analyses for the remaining confounding factors. Second, studies utilized different criteria for defining MetS. Most of the included studies have utilized NCEP-ATP-III and IDF criteria. The differences in cut points of each criterion might affect the outcomes. Third, due to limited data, we could not conduct the meta-analysis regarding the association between LBP levels and MetS. Fourth, it should be acknowledged that excluding studies published in languages other than English could lead to language bias, representing a potential limitation of this review. Finally, although we attempted to include all relevant studies, the possibility of publication bias cannot be completely ruled out, particularly given the tendency to publish studies with significant findings.

Conclusion

Results of the current study reflect a higher level of LBP among MetS cases compared to non-MetS participants. Although some inconsistencies were observed between subgroups—particularly in terms of diagnostic criteria and geographic region—the overall trend supports a potential association between elevated LBP levels and MetS. These discrepancies highlight the need for cautious interpretation and underscore the importance of standardized methodologies in future research. Besides, serum LBP levels were significantly associated with an increased risk of MetS. These findings support the fact that endotoxemia may contribute to the pathogenesis of insulin resistance and MetS through low-grade systemic inflammation. However, due to the high heterogeneity observed across studies, the influence of individual studies on the overall results, and the possibility of publication bias, these findings should be interpreted with caution. Further, longitudinal studies are needed to evaluate the prognostic and diagnostic accuracy of LBP for MetS risk. Additionally, it remains unclear whether LBP could be a good therapeutic option for MetS.

Data availability

The dataset analyzed during the current study is available from the corresponding author upon reasonable request.

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Acknowledgements

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Authors and Affiliations

  1. Child Growth and Development Research Center, Research Institute for Primordial Prevention of Non-Communicable Disease, Isfahan University of Medical Sciences, Isfahan, Iran

    Sadegh Mazaheri-Tehrani, Motahar Heidari-Beni & Roya Kelishadi

  2. Student Research Committee, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran

    Sadegh Mazaheri-Tehrani

  3. Zoonoses Research Center, Jahrom University of Medical Sciences, Jahrom, Iran

    Fatemeh Rezaei

  4. School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran

    Sara Heidari-Hasanabadi & Mohammadreza Malakoutikhah

  5. Heart Failure Research Center, Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran

    Reza Amani-Beni

  6. Department of Natural Sciences, School of Science and Technology, University of Georgia, Athens, Tbilisi, 0171, Georgia

    Mehrnoosh Arefian

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  1. Sadegh Mazaheri-Tehrani
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Contributions

SM-T: Conceptualization; Data curation, Investigation, Methodology, Writing - original draft. FR: Formal analysis, Software, Writing - review & editing. MM: Data curation, Investigation, Writing - original draft. SH-H: Data curation, Investigation, Writing - original draft. RA-B: Data curation, Investigation, Writing - original draft. MA: Data curation, Investigation, Writing - review & editing MH-B: Conceptualization, Project administration, Supervision, Writing - review & editing. RK: Conceptualization, Project administration, Supervision, Writing - review & editing.

Corresponding authors

Correspondence to Motahar Heidari-Beni or Roya Kelishadi.

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Mazaheri-Tehrani, S., Rezaei, F., Heidari-Hasanabadi, S. et al. Serum lipopolysaccharide binding protein (LBP) and metabolic syndrome: a systematic review and meta-analysis. Diabetol Metab Syndr 17, 268 (2025). https://doi.org/10.1186/s13098-025-01847-w

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Keywords

Diabetology & Metabolic Syndrome

ISSN: 1758-5996

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