Background
The human intestinal tract is colonized with many microorganisms, including numerous bacteria, resulting in the highest microbial biomass in the human body of approximately 1.5 kg. Most of the gut microbiome consists of 30–40 species from 4 main phyla: Firmicutes (64%), Bacteroidetes (23%), Proteobacteria (8%), and Actinobacteria (3%) [
1,
2]. The variation in the gut microbiome may also be more important than the genetic diversity of the host [
3].
The microbiota in the gut helps the immune system develop and mature, and it also contributes to metabolic activities, including the digestion of dietary fibre and the production of vitamins [
4‐
6]. In contrast, the gut microbiota responds rapidly to dietary interventions after short- and long-term studies in healthy adults, since short-term consumption of specified diets and dietary fibre can alter the structure of the gut microbiota and thus human health [
3,
7]. Dysregulation of the gut microbiota can contribute to insulin resistance (IR), a key factor in the pathogenesis of metabolic disorders [
8‐
11], ultimately leading to conditions such as obesity, hyperlipidaemia, hypertension, and diabetes.
As a result, lower bacterial numbers and diversity are associated with lower metabolic health and IR [
8]. On the other hand, the gut microbiome is connected to the development of IR. It is regulated by genetic, environmental, and social factors such as diet and psychological stress [
3]. In addition, recent studies have shown that high-fat diets, particularly those concerning saturated fat and trans-fatty acid composition, are associated with the development of IR [
7,
12].
Research on the gut microbiota and IR via bibliometric techniques is not yet available in the literature. Furthermore, only a limited number of studies have been conducted to predict gut microbiota hotspots [
13‐
23] or insulin hotspots [
24,
25]. As part of our efforts to better understand research trends and hotspots in the gut microbiota and IR, we used VOSviewer to analyse bibliometric data from publications in the Scopus database, which contains data on the great majority of papers published in this area. Overall, our bibliometric study can help researchers explore prospective avenues for collaboration and understand the knowledge landscapes of the gut microbiota and the field of IR, the evolutionary process, and the research hotspots on this topic. In addition, this study should act as a wake-up signal to researchers, nutritionists, and physicians that the gut microbiota requires more attention in the field.
Discussion
The aim of this bibliometric analysis was to explore the trends in publications related to the gut microbiota and IR. Notably, the last five years have seen a significant surge in research output in this area. Beginning in the 2010 s, an increasing number of studies linked the gut microbiota to IR. This increase can be attributed primarily to substantial funding directed toward microbiota research starting in approximately 2015.
In this study, China emerged as the leading country in research on the gut microbiota and IR, contributing to 30.5% of the publications, followed by the USA, with 20.23%. This aligns with the findings and proportions reported in earlier analyses. The data suggest that funding availability may play a key role in driving a country’s research output. Both China and the United States have ranked among the top three most productive nations globally over the past decade, and their institutions are among the top 10 funding sponsors. Specifically, China’s research productivity may be attributed to initiatives such as the launch of the Chinese Academy of Sciences’ Microbiome Program in 2017 [
57,
58] and the second phase of the National Institutes of Health’s Integrative Human Microbiome Project in 2013 [
59], both of which attracted significant scholarly interest and provided substantial financial support.
Compared with prior mappings, our analysis differs in scope, database strategy, and topical resolution. The Frontiers in Medicine study [
60] surveyed a broader window (2000–2024) and combined Web of Science and Scopus, querying “Gastrointestinal Microbiome” and “Insulin Resistance” in titles or abstracts, and emphasized collaborative networks and mechanism-themed hotspots such as short-chain fatty acids and gut hormones; it reported 1,884 records and highlighted productive outlets and authorship hubs (e.g., Food & Function, Nieuwdorp) rather than deriving a compact translational framework. In contrast, Tian et al. [
61]. (Journal of Diabetes & Metabolic Disorders, 2013–2022; WoSCC only; 4,749 records) used multiple tools (bibliometrix/CiteSpace/VOSviewer) and documented rapid growth led by China and the United States, with trend topics including the serum metabolome and natural products (e.g., resveratrol, flavonoids). Building on these broader portraits, our Scopus-based, IR title-anchored query (2015–2024) intentionally trades recall for topical precision, yielding a smaller but more focused corpus and a reproducible three-cluster structure—the HFD gut–liver axis (C1), patient-centered epidemiology/trials (C2), and inflammatory/metabolic signalling (C3)—that organizes mechanisms, preclinical models, and human interventions into a translational continuum and directly informs the clinical and trial design implications we propose.
Three key research areas concerning the relationship between the gut microbiota and IR were identified and analysed. Among these factors, mechanistic mediators and inflammatory signalling for the gut microbiota in IR have emerged as major focuses and have gained considerable attention. Current mechanistic work dissects how short-chain fatty acids (SCFAs) and inflammatory mediators interface with host metabolism. In HFD-fed mice, oat β-glucan restored circadian clock gene expression, increased colonic butyrate, and reversed IR, highlighting diet–microbe–clock crosstalk as a modifiable pathway [
62]. Parallel investigations have shown that fibroblast growth factor-21 therapy increases SCFA-producing taxa and bile acid signalling, lowering lipopolysaccharide levels and increasing Akt phosphorylation in diabetic mice [
63]. Collectively, these studies position SCFA-activated GPCRs, inflammatory cytokines (e.g., TNF-α) and bile acid receptors as convergent nodes for drug and nutritional interventions aimed at improving insulin sensitivity. Micronutrients play crucial roles in regulating hormone activity and host metabolism, with several micronutrients linked to the risk and progression of type 2 diabetes. Diets rich in minerals, trace elements, and vitamins can influence blood glucose levels and cellular glucose metabolism. Within the gut, dietary factors; microorganisms; and the host’s immune, endocrine, and metabolic systems interact. There is increasing interest in how macronutrients affect the host-microbe relationship in metabolic diseases. The balance between the host and microbiota, which influences the body’s glucose regulation, can be altered by micronutrients [
64]. Moreover, the gut microbiota processes nutrients to produce metabolites critical for host metabolism. Diets rich in cornstarch, branched-chain amino acids, fructose, soybean oil, or lard led to distinct microbiota profiles and influenced glucose metabolism. This change in glucose metabolism could also be partially replicated by transferring the microbiota [
65].
Another topic that has received much attention is “
patient-centred epidemiology and trials”. Clinical momentum has shifted from associative cohort work to intervention trials that directly manipulate the microbiome in insulin-resistant individuals. A double-blind phase II study revealed that single colonoscopic faecal microbiota transplantation (FMT) from lean donors significantly improved insulin sensitivity and reduced hepatic fat in adults with severe obesity and IR, outperforming placebo at 12 weeks [
66]. A 2024 umbrella meta-analysis further confirmed that microbiome-modulating therapeutics—probiotics, prebiotics, synbiotics and FMT—lower fasting glucose and insulin across metabolic syndrome populations, although larger trials are still needed to guide precision prescribing [
67]. Despite extensive studies of diabetes and the gut microbiota, we are still in the early stages of determining the precise involvement of the intestinal microbiota in diabetes mellitus [
68‐
71]. To date, we have commonly based our views on rodent data, yet the mouse microbiota differs greatly from the human microbiota. In addition, retrospective and observational research has not allowed an exact study of the causal association between the gut microbiota and diabetes development. The gut microbiota may play a role in the development of type 2 diabetes by altering glucose homeostasis and IR in key metabolic organs, such as fat, muscle, and liver [
72,
73]. Additionally, the gut microbiota may play a role in the digestion of sugars and the synthesis of gut hormones that regulate this process [
73]. Randomized microbiota-targeted trials now demonstrate tangible metabolic benefits. In a double-blind study, lean donor faecal microbiota transplantation increased insulin sensitivity and lowered hepatic fat in adults with metabolic syndrome within six weeks [
54]. Supplementation with pasteurized
Akkermansia muciniphila for three months improved HOMA-IR and reduced insulinemia in overweight, insulin-resistant subjects [
74]. Moreover, sulforaphane-rich broccoli-sprout extract alleviated NAFLD-related IR by enriching
Bacteroides/Lactobacillus, increasing colonic SCFA production and activating the GPR41/43-GLP-1 axis [
75]. Collectively, these patient-centred interventions validate the translational relevance of Cluster 2 and highlight microbial–metabolite pathways as actionable therapeutic targets.
Another hot topic is the
high-fat diet–gut–liver axis. Animal studies continue to show that high-fat diets (HFDs) reshape the intestinal microbiota in ways that aggravate hepatic steatosis and whole-body IR [
76,
77]. Many studies have linked obesity and metabolic problems to the promotion of dysbiosis caused by a HFD [
12,
78]. Research has shown that obese and overweight people have lower microbial diversity, which is associated with more severe dysmetabolism [
79,
80]. Enhanced intestinal permeability and inflammation may play a role in this outcome, as may an increased ability to harvest and store energy [
12]. The development of obesity, IR, and diabetes in the host is linked to altered microbiota composition through a number of mechanisms, including increased food energy intake, altered fatty acid metabolism and composition in adipose tissue and the liver, activation of the lipopolysaccharide toll-like receptor-4 axis of the lipopolysaccharide, modulation of the gut peptide YY and secretion of glucagon-like peptide (GLP)−1, and modulation of intestinal barrier integrity [
81].
The primary research priorities in the areas of the gut microbiota and IR align with the findings presented in the most frequently cited publications. These highly cited works offer significant insights, paving the way for further exploration across multiple research domains.
A notable example is Pedersen et al. [
49]., whose large-scale human cohort study linked specific microbial taxa and circulating branched-chain amino acids to IR, firmly situating this work in Cluster 2 (patient-centered epidemiology and clinical trials). In addition to these clinical insights, preclinical investigations, such as those of Anhê et al. [
53]. and Khan et al. [
52]., model Cluster 1 as the “high-fat-diet gut–liver axis,” showing that dietary or nutraceutical interventions that enrich
Akkermansia or rebalance bile acid metabolism can reverse HFD-induced steatosis and improve glucose homeostasis. Finally, mechanistic papers grouped under Cluster 3 (inflammatory and metabolic signalling)—for example, Canfora et al. [
51]. on short-chain fatty acids and Saad et al. [
46]. on LPS/TNF-α pathways—clarify how microbial metabolites and proinflammatory cytokines converge on insulin signalling nodes such as GPR41/43 and Akt. Together, these three thematic clusters, echoed by the most-cited studies in Table
5, delineate a translational continuum that runs from molecular mechanisms (Cluster 3) through diet-induced animal models (Cluster 1) to human observational and interventional research (Cluster 2), thereby charting the current roadmap for gut microbiota-driven strategies to combat IR.
Despite rapid progress, several gaps warrant attention. Cross-study comparability is constrained by heterogeneity in dietary protocols (fibre types and doses, timing), probiotic/next-generation candidate specifications (strain identity, dose, viability), and FMT donor characterization, underscoring the need for harmonized, CONSORT-style reporting of microbiome interventions. Causal understanding remains limited by the infrequent use of prespecified mediation analyses and incomplete integration of multiomics pipelines that trace pathways from diet, through microbial changes and metabolites, to host receptors and insulin resistance end points. Time-varying and contextual modifiers—including circadian timing, concomitant antibiotics/PPIs/antidiabetic agents, and habitual diet—are often undermeasured but are likely to shape intervention effects. Generalizability is further limited by the underrepresentation of diverse populations and LMIC settings, where dietary and environmental exposures differ substantially. Evidence on durability and safety, particularly for FMT and strain-level biotherapeutics, remains sparse beyond 12–24 weeks. Finally, systematically charting temporal shifts in study designs (animal vs. human; observational vs. interventional) and assessing methodological rigor will require standardized manual coding and formal risk-of-bias appraisal—priorities for future mapping studies that complement bibliometric insights.
Implications for clinical practice and future research
Our literature mapping into three translationally connected clusters—HFD gut–liver axis (C1), patient-centric epidemiology/trials (C2), and inflammatory/metabolic signalling (C3; in Table
6)—justifies a conservative, adjunctive clinical approach and a research agenda. In the clinic, clinicians should proceed with guideline-directed management of insulin resistance and comorbidities but counsel high-fibre, plant-rich eating styles consistent with SCFA- and bile acid–common mechanism signals in C3 and HFD-modulating signals in C1. Currently, strain-specific probiotics, next-generation contenders (e.g.,
Akkermansia muciniphila), and fecal microbiota transplantation should be restricted until efficacy, dose, durability, and safety are established. In accordance with the transition identified in C2, subsequent research should be weighted in favour of mechanism-anchored randomized trials with biomarker-guided stratification (e.g., baseline HOMA-IR, enterotypes), standard reporting of intervention (diet composition and schedule; strain identity and viability; donor screening), longer follow-up to validate durability, and incorporation of diverse populations to increase generalizability. Pragmatic comparative-effectiveness trials alongside routine care, in combination with multiomic cohorts and planned mediated analyses, will translate evidence in bibliometric into actionable knowledge. Owing to database coverage, keywords chosen, and citation time lags, hotspots identified should be interpreted best as indicative signals to inform trial design and research priorities, not as definitive clinical recommendations.
Strengths and limitations
To our knowledge, using the Scopus database, this bibliometric study is the first to analyse the characteristics of the gut microbiota and IR-related articles published from 2015 to 2024. However, certain limitations should be mentioned. First, the current study used the Scopus database, one of the most widely used resources for researchers in bibliometric analysis. Although Scopus offers broad, interdisciplinary coverage and robust author keyword indexing—assets for term-mapping analyses—it differs from Web of Science (WoS) in terms of journal selection, historical depth, and citation graph construction. Prior comparisons indicate partially overlapping but nonidentical coverage across WoS and Scopus; hence, absolute counts and rankings can vary by database. Given the practical constraints in harmonizing exports across platforms for VOSviewer mapping, we base our analysis on Scopus, acknowledging that multidatabase triangulation could further increase completeness. Second, the publications that have been published for a considerable amount of time are the ones that are cited the most frequently. As a result, some recently released high-quality studies cannot be assessed by us since they do not receive sufficient citations. Third, the dataset is predominantly English-language, reflecting Scopus coverage and the search strategy; non-English outputs may be underrepresented, potentially attenuating signals from some regions and journals. Fourth, false positive and false negative results are inherent challenges, regardless of the precision of the search strategy. However, we believe that the occurrence of such results was minimal and had little to no impact on the overall accuracy of our study’s findings. By focusing the search strategy on article titles, we increased the accuracy and reduced the likelihood of false positives. While one could argue against this approach, we felt it would be unjust to include every article containing the keyword “insulin resistance” in the title, abstract, or keywords. Therefore, restricting the search query to the article title improved the precision of the retrieved articles. Fifth, the current study used a thorough list of keywords related to the gut microbiota and IR based on those found in prior studies; nonetheless, it is probable that some keywords were omitted, which may have led to false-negative results. Sixth, the lists of important active players were taken directly from Scopus when retrieved. The amount of research produced by particular countries, funding agencies, or institutions might occasionally be underestimated in the Scopus database owing to multiple variations in the names or spellings of these entities. Seventh, bibliometric methods map volume, influence, and topic structure but do not assess the risk of bias or methodological rigor. Future systematic reviews/scoping reviews are needed to qualify the evidentiary strength of the clusters we identify. Finally, when searching at different points in time, the citation times of the publications are different; therefore, it is vital to update them for future studies. Despite our efforts to ensure consistency in the data retrieval process, the search period was limited to publications between 2015 and 2024, with data retrieval completed on June 15, 2025. While we used a PUBYEAR < 2025 filter to exclude post-2024 papers, any recent publications that have emerged since the retrieval date were not included in this study. Additionally, 2025 was excluded from the analysis because the year is still open for new issues and is not yet complete. Future studies should consider updating the results to account for new publications beyond the search cutoff.