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Peer-reviewedCC BY-NC-ND 4.0Diabetology & Metabolic Syndrome

Dietary index for gut microbiota and risk of metabolic syndrome: the mediating role of hepatic steatosis in a prospective cohort study

5 affiliations
  1. 1Department of Nutrition, SR.C., Islamic Azad University, Tehran, Iran
  2. 2Department of Nutrition, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
  3. 3Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran
  4. 4Faculty of Nutrition Sciences and Food Technology, National Nutrition and Food Technology Research Institute (WHO Collaborating Center), Shahid Beheshti University of Medical Sciences, P. O. 19395- 4741, Tehran, Iran
  5. 5Nutrition and Health Research Center, Nasim Institute, Tehran, Iran

Abstract

Background: Metabolic syndrome (MetS) is a growing public health concern, with emerging evidence implicating that gut microbiota plays a role in MetS pathogenesis. The Dietary Index for Gut Microbiota (DI-GM) quantifies diet quality in relation to microbial diversity. This study examined the association between DI-GM and MetS risk, evaluating hepatic steatosis as a potential mediator.

Methods: This prospective cohort included 4,503 adults (20–70 years) from the Monitoring of Metabolic Diseases Risk Factors in Tehran (MMRT) study, followed over five years. Dietary intake was assessed using a validated 125-item food frequency questionnaire to calculate DI-GM scores. Hepatic steatosis was quantified via controlled attenuation parameter (CAP) using transient elastography. MetS was defined according to Adult Treatment Panel III criteria. Multivariable logistic regression and mediation analyses evaluated associations.

Results: Higher DI‑GM scores were associated with lower MetS incidence. In the fully adjusted model (Model 2), participants in the highest DI‑GM quartile had a 66% lower odds of MetS compared with the lowest quartile (OR = 0.34; 95% CI: 0.27–0.43; P‑trend < 0.001). Each one‑unit increase in the DI‑GM score was associated with an 18% decrease in the odds of MetS (OR = 0.82; 95% CI: 0.78–0.85; P < 0.001). All five MetS components showed significant inverse associations, with the strongest effects observed for elevated waist circumference, hypertriglyceridemia, and low high‑density lipoprotein cholesterol. In mediation analysis, hepatic steatosis accounted for approximately 65% of the DI‑GM–MetS association (indirect effect: −0.0263; P < 0.01), although causal interpretation is limited by the observational design.

Conclusion: Greater adherence to a gut microbiota-supportive diet, as measured by DI-GM, is associated with a reduced risk of MetS, largely mediated by reductions in hepatic fat. These findings highlight the potential of microbiome-oriented dietary interventions for MetS prevention.

Graphical abstract:

Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1186/s13098-026-02255-4.

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BibTeX
@article{etesami2026dietary,
  title = {{Dietary index for gut microbiota and risk of metabolic syndrome: the mediating role of hepatic steatosis in a prospective cohort study}},
  author = {Elahe Etesami and Farzam Kamrani and Ali Nikparast and Matin Sepehrinia and Reza Homayounfar and Jalaledin Mirzay Razzaz},
  journal = {Diabetology \& Metabolic Syndrome},
  year = {2026},
  month = jul,
  doi = {10.1186/s13098-026-02255-4},
  url = {https://doi.org/10.1186/s13098-026-02255-4},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - Dietary index for gut microbiota and risk of metabolic syndrome: the mediating role of hepatic steatosis in a prospective cohort study
AU  - Elahe Etesami
AU  - Farzam Kamrani
AU  - Ali Nikparast
AU  - Matin Sepehrinia
AU  - Reza Homayounfar
AU  - Jalaledin Mirzay Razzaz
PY  - 2026
DA  - 2026/07/31
JO  - Diabetology & Metabolic Syndrome
DO  - 10.1186/s13098-026-02255-4
UR  - https://doi.org/10.1186/s13098-026-02255-4
AB  - Background: Metabolic syndrome (MetS) is a growing public health concern, with emerging evidence implicating that gut microbiota plays a role in MetS pathogenesis. The Dietary Index for Gut Microbiota (DI-GM) quantifies diet quality in relation to microbial diversity. This study examined the association between DI-GM and MetS risk, evaluating hepatic steatosis as a potential mediator.  Methods: This prospective cohort included 4,503 adults (20–70 years) from the Monitoring of Metabolic Diseases Risk Factors in Tehran (MMRT) study, followed over five years. Dietary intake was assessed using a validated 125-item food frequency questionnaire to calculate DI-GM scores. Hepatic steatosis was quantified via controlled attenuation parameter (CAP) using transient elastography. MetS was defined according to Adult Treatment Panel III criteria. Multivariable logistic regression and mediation analyses evaluated associations.  Results: Higher DI‑GM scores were associated with lower MetS incidence. In the fully adjusted model (Model 2), participants in the highest DI‑GM quartile had a 66% lower odds of MetS compared with the lowest quartile (OR = 0.34; 95% CI: 0.27–0.43; P‑trend < 0.001). Each one‑unit increase in the DI‑GM score was associated with an 18% decrease in the odds of MetS (OR = 0.82; 95% CI: 0.78–0.85; P < 0.001). All five MetS components showed significant inverse associations, with the strongest effects observed for elevated waist circumference, hypertriglyceridemia, and low high‑density lipoprotein cholesterol. In mediation analysis, hepatic steatosis accounted for approximately 65% of the DI‑GM–MetS association (indirect effect: −0.0263; P < 0.01), although causal interpretation is limited by the observational design.  Conclusion: Greater adherence to a gut microbiota-supportive diet, as measured by DI-GM, is associated with a reduced risk of MetS, largely mediated by reductions in hepatic fat. These findings highlight the potential of microbiome-oriented dietary interventions for MetS prevention.  Graphical abstract:  Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1186/s13098-026-02255-4.
SN  - 1758-5996
ER  -