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SARCOPENIA AND IBD: MOLECULAR AND MICROBIAL PATHWAYS AND POTENTIAL PHARMACOLOGICAL MODULATORS IN EXPERIMENTAL MODELS OF CHRONIC INFLAMMATORY BOWEL DISEASE

Valentina Petito 1, Sara Troisi 1, Letizia Masi 1, Valeria Emoli 2, Loris Riccardo Lopetuso 1, Federica Di Vincenzo 2, Pierluigi Puca 2, Ivan Capobianco 2, Antonio Gasbarrini 2,3, Franco Scaldaferri 1,4

Affiliations

1 Department of Medical and Surgical Sciences, IBD unit, Center for Diseases of Digestive System (CeMAD), Fondazione Policlinico Universitario "A. Gemelli" IRCCS, Rome, Italy

2 Department of Translational Medicine and Surgery, Catholic University of the Sacred Heart, Rome, Italy

3 Department of Medical and Surgical Sciences, IBD unit, Center for Diseases of Digestive System (CeMAD), Fondazione Policlinico Universitario "A. Gem

4 Department of Translational Medicine and Surgery, Catholic University of the S

Summary

AI Generated

A DSS-induced colitis mouse model and in vitro myoblast studies demonstrate that gut dysbiosis, LPS, and inflammatory cytokines contribute to sarcopenia in IBD through activation of muscle atrophy pathways, with JAK inhibitors showing partial protective effects.

The colitic mouse model exhibited reduced body weight and muscle performance, increased expression of muscle atrophy markers (myostatin and Murf-1), elevated STAT3-pSTAT3 pathway expression, decreased pAKT, gut dysbiosis, and increased serum LPS.
In vitro treatment of C2C12 myoblasts with Upadacitinib and Tofacitinib in the presence of inflammatory cytokines (TNF-α, IFN-γ, IL-6) decreased expression of muscle atrophy pathways (STAT3, pSTAT3, NFkB) and increased pAKT expression.
When myoblasts were treated with LPS, NFkB expression did not decrease with drug addition, suggesting that LPS activates NFkB independently of the JAK/STAT pathway and is only partially controlled by these drugs.
The authors propose that microbiota and LPS should be considered alongside inflammatory cytokines in the pathogenesis of sarcopenia in IBD, representing a gut-muscle axis warranting further investigation.

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Abstract

Introduction

Sarcopenia is a syndrome characterized by the progressive and generalized loss of skeletal muscle mass. Primary sarcopenia is associated with the aging process, while the secondary one is caused by several factors including inflammatory conditions, such as inflammatory bowel disease (IBD). Since there is a complex interaction between inflammation, intestinal dysbiosis and malnutrition which lead to muscle degeneration in IBD patients, it is referred to as the gut-muscle axis. In particular, the high level of cytokines and the gut dysbiosis which characterizes IBD is responsible for the activation of pathways that cause an imbalance in muscle protein synthesis. However, the involvement of molecular and microbial mechanisms of sarcopenia, at present, has not been extensively studied in IBD.

Aims & Methods

In order to identify the mechanisms that are potentially involved in the onset of sarcopenia, a DSS-induced colitis mouse model has been created. To ensure that the model developed sarcopenia, we performed physical performance assessment at rotarod. On this well-characterized model, we studied the muscle by immunohistochemistry, by fiber count per field and by Cross Sectional Area. Next, we evaluated the gut microbiota and serum LPS detection. In vitro, with the aim to create a situation of intestinal inflammation and to assess the activation of pathways of muscle atrophy, we used the immortalized murine myoblast cell line C2C12 at different time points, 30'-2h-6h. Treatments performed included pro-inflammatory cytokines (TNF-α, IFN-γ, IL-6), LPS and drugs (Infliximab, Upadacitinib, Tofacitinib) in order to assess cellular response to the most promising drugs used in the treatment of IBD.

Results

The mouse model showed a reduction in body weight and muscle performance, probably associated with quantitative and qualitative alterations in muscle fibers. In addition, increased expression of markers of muscle atrophy (myostatin and Murf-1) was found in colitic mouse muscle. Also we observed increasing expression of the pathway STAT3-pSTAT3 involved in muscle wasting and decreasing pAKT, which is associated with muscle growth. Most relevant, a condition of dysbiosis was found in the colitic model, as well as increased LPS in the serum of mice.
In vitro, Upadacitinib and Tofacitinib in the presence of inflammatory cytokines decrease the expression of muscle atrophy-associated pathways (STAT3, its active form pSTAT3, and the transcriptional factor NFkB) and increase the expression of pAKT, a protein associated with muscle synthesis. When cells were treated with LPS, NFkB expression did not decrease with drug addition, suggesting that LPS is able to activate NFkB independently of the JAK/STAT pathway.

Conclusion

These data open new scenario for the gut-muscle axis as a promising area of research for the management of sarcopenia in IBD. Therefore, we might also consider the role of microbiota and LPS in addition to inflammatory cytokines in the pathogenesis of sarcopenia in IBD, since LPS-induced signaling is only partially controlled by drugs.

Conference

UEG Week Copenhagen 2023

Topics

IBD

Submission format

Abstract

Session

PP 05 IBD (Posters)

Citation

United European Gastroenterology Journal 2023; 11 (Supplement 8)

Published

2023

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DIET QUALITY AND DIVERSITY IN CHILDHOOD AND ADOLESCENCE AND LATER RISK OF INFLAMMATORY BOWEL DISEASE: A TRI-NATIONAL BIRTH COHORT STUDY

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DIET QUALITY AND DIVERSITY IN CHILDHOOD AND ADOLESCENCE AND LATER RISK OF INFLAMMATORY BOWEL DISEASE: A TRI-NATIONAL BIRTH COHORT STUDY

Annie Guo 1, Ida Sigvardsson 1, Sabine Jansson 2,3, Henrik Imberg 4,5, Anne Lise Brantsæter 6, Anne Vibeke Wewer 7,2,3, Johnny Ludvigsson 8,9, Ketil Størdal 10,11, Mikkel Malham 3,2, Karl Mårild 12,1

Affiliations

1 University of Gothenburg, Gothenburg, Sweden

2 Hvidovre Hospital, Hvidovre, Denmark

3 Copenhagen University Hospital, Hvidovre, Denmark

4 Statistiska Konsultgruppen Sweden AB, Gothenburg, Sweden

5 University of Gothenburg, Gothenburgsw, Sweden

6 Norwegian Institute of Public Health, Oslo, Norway

7 Copenhagen University Hospital, Hvidovre, Hvidovre, Denmark

8 Crown Princess Victoria Children’s Hospital, Linköping, Sweden

9 Linköping University, Linköping, Sweden

10 Oslo University Hospital, Oslo, Norway

11 University of Oslo, Oslo, Norway

12 Queen Silvia Children’s Hospital, Gothenburg, Sweden

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Abstract

Introduction

Diet influences the gut microbiome composition and immune system development across the lifespan.^{1, 2} While a high diet quality in the first year of life has been associated with a reduced risk of later IBD,³ the impact of diet in school age and adolescence on IBD risk remains largely unexplored.

Aims & Methods

The aim was to investigate the associations between diet quality and diversity in childhood and adolescence and later risk of inflammatory bowel disease (IBD). We followed individuals born in 1996–2009 from three population-based birth cohorts (The Norwegian Mother, Father and Child Cohort Study, the Danish National Birth Cohort, and All Babies in Southeast Sweden). The primary outcome was IBD, and the time of event was defined as the first of at least two diagnostic codes for IBD in linked national patient registers by 2022. Dietary exposures were measured using repeated questionnaires: diet quality at ages 7–8 and 11–14 years was measured using a modified Healthy Eating Index, and diet diversity at age 11–14 years was assessed using a Diet Diversity Score. Each dietary exposure was modeled into low, medium, and high based on tertiles. Cohort-specific adjusted hazard ratios (aHRs) and 95% confidence intervals (CIs) for developing IBD, Crohn’s disease (CD), and ulcerative colitis (UC) were estimated using Cox proportional hazards regression adjusted for sex, IBD heredity, and socioeconomic status, pooled across cohorts using a random-effects model. Joint modeling was conducted to account for the repeated diet quality measurements and their association with time to IBD development.

Results

We followed 137,179 individuals for 1,894,582 person-years. During this time, 811 developed IBD. The pooled aHR for IBD comparing high vs low diet quality was 0.83 (95% CI 0.62–1.10) at ages 7–8, and 0.69 (0.51–0.93) at ages 11–14 (Table 1). Similar associations were observed for CD (ages 7–8: aHR=0.74 [0.45–1.21]; ages 11–14: aHR=0.66 [0.44–0.99]), but not for UC (ages 7–8, aHR=0.98 [0.73–1.31]; ages 11–14, aHR=0.71 [0.48–1.07]). For high vs low diet diversity at ages 11–14, the pooled aHRs were 0.76 (0.58–1.00) for overall IBD, 0.79 (0.49–1.26) for CD, and 0.74 (0.49–1.11) for UC. Joint modelling also showed that a higher overall longitudinal diet quality exposure was associated with a reduced risk of IBD (0.87 [0.78–0.97] and CD (0.87 [0.78–0.94], with largely similar estimates in the adjusted model.

	Inflammatory bowel disease		Crohn's disease
Exposure	HR (95% CI)	aHR (95% CI)	HR (95% CI)	aHR (95% CI)
Diet quality 7-8 years
Low	Reference	Reference	Reference	Reference
Medium	0.80 (0.67–0.95)	0.79 (0.66–0.94)	0.78 (0.60–1.01)	0.76 (0.58–0.99)
High	0.83 (0.64–1.08)	0.83 (0.62–1.10)	0.76 (0.47–1.22)	0.74 (0.45–1.21)
Diet quality 11-14 years
Low	Reference	Reference	Reference	Reference
Medium	0.83 (0.66–1.04)	0.83 (0.66–1.04)	0.84 (0.61–1.16)	0.83 (0.60–1.16)
High	0.69 (0.51–0.92)	0.69 (0.51–0.93)	0.66 (0.44–0.99)	0.66 (0.44–0.99)

Multiple imputation was applied to handle missing data. CI, confidence interval; HR, hazard ratio.

Conclusion

In this tri-national birth cohort study, higher diet quality in childhood and adolescence, particularly at 11–14 years of age, was associated with a lower risk of CD.

References

1. Lynch SV, Pedersen O. The Human Intestinal Microbiome in Health and Disease. N Engl J Med 2016;375:2369-2379.
2. Dong TS, Gupta A. Influence of Early Life, Diet, and the Environment on the Microbiome. Clinical Gastroenterology and Hepatology 2019;17:231-242.
3. Guo A, Ludvigsson J, Brantsæter AL, et al. Early-life diet and risk of inflammatory bowel disease: a pooled study in two Scandinavian birth cohorts. Gut 2024;73:590-600.

Event

UEG Week Barcelona 2026

Topics

Paediatrics Small Intestine & Nutrition IBD Gut Microbiota

Submission format

Abstract

Session

Beyond prescriptions: Improving IBD outcomes with non-pharmaceutical approaches

Citation

2026: United European Gastroenterology Journal 2026; 14 (S1)

Published

2026

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DIET QUALITY AND DIVERSITY IN CHILDHOOD AND ADOLESCENCE AND LATER RISK OF INFLAMMATORY BOWEL DISEASE: A TRI-NATIONAL BIRTH COHORT STUDY

Karl Mårild

CONSUMPTION OF ULTRA-PROCESSED FOOD PROMOTE INFLAMMATORY POTENTIAL OF FECAL MICROBIOME THROUGH ALTERING THE BALANCE OF TH17 AND RORYT TREG

Williams Turpin

FRUCTANS BOOST COLONIC FERMENTATION BUT DO NOT AGGRAVATE SYMPTOMS IN NON-CONSTIPATED IBS PATIENTS ON A LOW FODMAP DIET – A RANDOMIZED CONTROLLED TRIAL

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Stefania Vetrano

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UEG Presentation

New

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CONSUMPTION OF ULTRA-PROCESSED FOOD PROMOTE INFLAMMATORY POTENTIAL OF FECAL MICROBIOME THROUGH ALTERING THE BALANCE OF TH17 AND RORYT TREG

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CONSUMPTION OF ULTRA-PROCESSED FOOD PROMOTE INFLAMMATORY POTENTIAL OF FECAL MICROBIOME THROUGH ALTERING THE BALANCE OF TH17 AND RORYT TREG

Jeongseok Kim 1, Cong Phi Dang 2, Cathy McShane 1, Alyssa Waslyk 1, Qilong Li 1, Benoît Chassaing 3, Sun-Ho Lee 1,2, Ken Croitoru 1,2, Williams Turpin 1,2

Affiliations

1 Lunenfeld Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Canada

2 Temerty Faculty of Medicine, University of Toronto, Toronto, Canada

3 Institut Pasteur, Université Paris Cité, INSERM U1306, Paris, France

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Abstract

Introduction

Crohn’s disease (CD) is a chronic disorder of unknown etiology. Diet, particularly the consumption of ultra-processed foods (UPFs), has been implicated in CD development. Despite this, there is limited research examining how UPFs influence the mucosal immune response. Our study aims to (i) determine whether long-term UPF consumption alters the inflammatory potential of the gut microbiome and (ii) assess whether transfer of the microbiome from individuals consuming high amounts of UPFs affects intestinal T-cell populations in germ-free mice (GFMs).

Aims & Methods

Serum and stool samples collected prior to the onset of CD were obtained from the GEM project, a cohort of prospectively followed healthy first-degree relatives of CD patients. The microbiome was characterized by 16S rRNA sequencing of stool DNA, and serum protein profiles were measured using the Olink Proximity Extension Assay. For mouse experiments, human feces from high- or low-UPF consumers, defined as individuals with more than 40% of daily caloric intake derived from NOVA4 food items according to the NOVA classification, were transplanted into wild-type germ-free recipient mice fed either a standard chow diet or a Western diet. After four weeks of microbial colonization, lamina propria T-cell populations in the intestine, including RORγt⁺ Treg (CD4⁺RORγt⁺FoxP3⁺) and Th17 (CD4⁺RORγt⁺FoxP3⁻) cells, were analyzed using flow cytometry.

Results

Our study included 2,336 participants, including 1,977 from Canada and 359 from the United States. The mean proportion of total energy consumption from UPFs was 36.6 ±12.7%. Participants with higher UPF consumption showed significant difference in 36 serum proteins (q<0.007) compared with those with lower UPF consumers. Notably, immune-related proteins, including IL2RA, TNFRS9, TNFRSF11A, and CD4, were enriched in individuals with high UPF consumption. Microbiome analysis revealed that several taxa, predominantly from the Lachnospiraceae and Ruminococcaceae families, were associated with UPF consumption. In addition, the presence of Marvinbryantia was associated with an increased risk of CD among individuals with high UPF consumption. Mice receiving feces from high-UPF consumers exhibited reduced proportion of protective RORyt⁺ Treg cells in both the ileum and colon (p<0.001). Moreover, mice fed a Western diet (high in fat and simple sugars) and colonized with feces from high-UPF consumer showed a significantly higher proportion of Th17 cells in the colon than mice receiving feces from low-UPF consumers (p=0.023).

Conclusion

Our findings suggest that UPF consumption alters the inflammatory potential of the gut microbiome. Using gnotobiotic mice, we further demonstrated that UPF-associated microbial communities may induce an imbalance between RORγt⁺ regulatory T cells and Th17 cells. Together, these results suggest that the gut microbiome associated with high UPF consumption may contribute to CD onset through immune dysregulation and support the notion that dietary modulation of the microbiome could represent a potential strategy for CD prevention.

Disclosure

On half of the CCC-GEM Project Research Consortium
Funding agencies: CCC, CIHR, and Helmsley Charitable trust

Event

UEG Week Barcelona 2026

Topics

IBD Mechanisms & Personalised Medicine Immunology Gut Microbiota Small Intestine & Nutrition

Submission format

Abstract

Session

On bugs and food: New lessons in microbiomics and dietomics in IBD

Citation

2026: United European Gastroenterology Journal 2026; 14 (S1)

Published

2026

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DIET QUALITY AND DIVERSITY IN CHILDHOOD AND ADOLESCENCE AND LATER RISK OF INFLAMMATORY BOWEL DISEASE: A TRI-NATIONAL BIRTH COHORT STUDY

Karl Mårild

CONSUMPTION OF ULTRA-PROCESSED FOOD PROMOTE INFLAMMATORY POTENTIAL OF FECAL MICROBIOME THROUGH ALTERING THE BALANCE OF TH17 AND RORYT TREG

Williams Turpin

FRUCTANS BOOST COLONIC FERMENTATION BUT DO NOT AGGRAVATE SYMPTOMS IN NON-CONSTIPATED IBS PATIENTS ON A LOW FODMAP DIET – A RANDOMIZED CONTROLLED TRIAL

Magnus Simrén

Ostomy management

Revital Barkan

HIGH ADHERENCE TO THE MEDITERRANEAN DIET DELAYS SURGERY AND REPROGRAMS INTESTINAL CELLULAR STATES IN CROHN’S DISEASE

Stefania Vetrano

Evidence of disordered eating in disorders of gut–brain interaction

Chloé Melchior

UEG Presentation

New

Share via Email Share on Facebook Share on X Share on LinkedIn Share on Bluesky

FRUCTANS BOOST COLONIC FERMENTATION BUT DO NOT AGGRAVATE SYMPTOMS IN NON-CONSTIPATED IBS PATIENTS ON A LOW FODMAP DIET – A RANDOMIZED CONTROLLED TRIAL

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FRUCTANS BOOST COLONIC FERMENTATION BUT DO NOT AGGRAVATE SYMPTOMS IN NON-CONSTIPATED IBS PATIENTS ON A LOW FODMAP DIET – A RANDOMIZED CONTROLLED TRIAL

Joost Algera 1,2, Chloé Melchior 3,1, Jenny Lövdahl 2,1, Kristina Cullman 1, Amanda Blomsten 1, Sanna Nybacka 1, Stine Störsrud 2,1, Hans Törnblom 1,2, Magnus Simrén 1,2,4

Affiliations

1 Sahlgrenska Academy, University Of Gothenburg, Gothenburg, Sweden

2 Sahlgrenska University Hospital, Gothenburg, Sweden

3 Rouen University Hospital, INSERM U1073, CIC-CRB-1404, Rouen, France

4 University of North Carolina, Chapel Hill, United States

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Abstract

Introduction

Fermentable oligo-, di-, monosaccharides and polyols (FODMAP) may provoke gastrointestinal (GI) symptoms through physiological mechanisms in patients with irritable bowel syndrome (IBS)¹, and fructans have been suggested to be of particular importance². Negative expectations can exacerbate symptoms (nocebo effects)³ but the extent to which food components aggravate symptoms through physiological processes versus the contribution of patients' expectations of symptoms remains unclear.

Aims & Methods

We aimed to assess the link between GI symptoms, fructan intake, and colonic fermentation using an ingestible gas-sensing capsule and breath tests in patients with non-constipated (diarrhea-predominant and mixed) IBS on a low FODMAP diet.
Non-constipated IBS patients (Rome IV, n=89, age 18–50 years, 83% females) were included in this randomized, placebo-controlled trial (NCT04830410). Baseline assessment was made while patients retained their habitual diet. Next, the patients adhered to a low FODMAP diet for three weeks with all foods provided. During week 3, patients were challenged with fructans or maltodextrin (sham), with either high (18g; 6g tds, n=24) or low dosages (6g; 2g tds, n=65).
Patients reported severity of GI (IBS-SSS) at baseline and at the end of week 2 and 3, as well as stool form (BSFS) for all bowel movements. Colonic fermentation was assessed at baseline and at the end of week 3: luminal colonic hydrogen and carbon dioxide concentrations (overall and regional [per quartile of colonic transit time]) were measured using a gas-sensing capsule⁴, with breath concentrations of hydrogen and methane concentrations also examined. The gas-sensing capsule also provided whole gut and segmental transit times.

Results

The low FODMAP diet reduced overall IBS symptom severity at the end of week 2 compared to the habitual diet (IBS-SSS; mean change = -89 ± 94, P<0.0001), as well as individual symptoms P<0.0001 for all). Moreover, the low FODMAP diet reduced the frequency of loose stools at the end of week 2 (% loose stools; mean change 10% ± 19%, P<0.0001).
At the end of week 3, no significant differences in symptoms or transit times were observed between the fructans and sham challenges. This was observed for both 18g and 6g interventions (Table). Breath hydrogen and methane were higher in the 18g fructans group compared with sham (P<0.01 for both). Luminal hydrogen concentration (overall and in quartile 4) was higher in the 18g fructans group compared with sham (P=0.03 and P=0.04) while there were no differences in carbon dioxide concentrations. No differences in colonic fermentation were observed between the 6g fructans and sham groups.
In the 6g population, the intervention period increased overall IBS symptom severity, independent of fructans or sham intervention [ß-coefficient: 37 (95% CI: 5-70), p=0.03].

Table 1. Fructans vs. sham	18 g Fructans (n=12)	18 g Sham (n=12)	6 g Fructans (n=32)	6 g Sham (n=33)
IBS-SSS Total Pain intensity Pain frequency Abdominal distension Bowel habit dissatisfaction Daily life interference	210 ± 93 35 ± 25 28 ± 33 43 ± 35 49 ± 15 55 ± 19	173 ± 104 24 ± 21 32 ± 34 25 ± 20 44 ± 24 50 ± 27	200 ± 123 31 ± 28 36 ± 36 35 ± 35 44 ± 21 54 ± 26	223 ± 101 40 ± 27 39 ± 32 38 ± 30 49 ± 22 57 ± 24
BSF Loose stools, % BSF Normal stools, % BSF Hard stools, %	14 ± 14 59 ± 30 10 ± 13	22 ± 27 67 ± 27 10 ± 17	14 ± 22 69 ± 28 17 ± 22	18 ± 23 69 ± 27 10 ± 12
Colonic transit time (h) Whole gut transit time (h)	18.7 (15.6-39.4) 26.8 (24.2-35.3)	17.9 (16.0-18.9) 26.1 (24.3-28.3)	21.8 (14.6-40.1) 28.6 (23.5-50.8)	23.4 (14.6-36.6) 32.5 (25.0-50.0)
Overall luminal H2, % Overall luminal CO2, %	6.93 ± 3.88 * 19.34 ± 4.40	3.10 ± 2.33 16.65 ± 3.38	6.10 ± 3.43 24.44 ± 9.34	5.28 ± 4.37 25.71 ± 7.47
Breath H2, AUC (ppm) Breath CH4, AUC (ppm)	3399 ± 2432 * 1033 ± 698 *	1503 ± 434 529 ± 511	1740 ± 1944 658 ± 813	1693 ± 1504 890 ± 1142

Conclusion

In non-constipated IBS patients following a low FODMAP diet, supplementation with 18 g (but not 6 g) fructans per day led to increased colonic fermentation, without severe aggravation of GI symptoms. Independent of intervention, IBS symptom severity increased, highlighting the role of the nocebo effect. Central and peripheral processes may both be important in FODMAP-related symptoms with individual variations.

References

1. Ong DK, Mitchell SB, Barrett JS, Shepherd SJ, Irving PM, Biesiekierski JR, et al. Manipulation of dietary short chain carbohydrates alters the pattern of gas production and genesis of symptoms in irritable bowel syndrome. J Gastroenterol Hepatol. 2010;25(8):1366–73.
2. Van den Houte K, Colomier E, Routhiaux K, Mariën Z, Schol J, Van den Bergh J, et al. Efficacy and findings of a blinded randomized reintroduction phase for the low FODMAP diet in Irritable Bowel Syndrome. Gastroenterology. 2024 Jul;167(2):333-342.
3. Elsenbruch S. Unravelling the power of nocebo in symptom response to food challenge in irritable bowel syndrome. The Lancet Gastroenterology & Hepatology, 2025; 10, 780-781
4. Berean KJ, Ha N, Ou JZ, Chrimes AF, Grando D, Yao CK, et al. The safety and sensitivity of a telemetric capsule to monitor gastrointestinal hydrogen production in vivo in healthy subjects: a pilot trial comparison to concurrent breath analysis. Aliment Pharmacol Ther. 2018;48(6):646–54.

Event

UEG Week Barcelona 2026

Topics

Small Intestine & Nutrition Primary Care Colorectal

Submission format

Abstract

Session

Insights into IBS

Citation

2026: United European Gastroenterology Journal 2026; 14 (S1)

Published

2026

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DIET QUALITY AND DIVERSITY IN CHILDHOOD AND ADOLESCENCE AND LATER RISK OF INFLAMMATORY BOWEL DISEASE: A TRI-NATIONAL BIRTH COHORT STUDY

Karl Mårild

CONSUMPTION OF ULTRA-PROCESSED FOOD PROMOTE INFLAMMATORY POTENTIAL OF FECAL MICROBIOME THROUGH ALTERING THE BALANCE OF TH17 AND RORYT TREG

Williams Turpin

FRUCTANS BOOST COLONIC FERMENTATION BUT DO NOT AGGRAVATE SYMPTOMS IN NON-CONSTIPATED IBS PATIENTS ON A LOW FODMAP DIET – A RANDOMIZED CONTROLLED TRIAL

Magnus Simrén

Ostomy management

Revital Barkan

HIGH ADHERENCE TO THE MEDITERRANEAN DIET DELAYS SURGERY AND REPROGRAMS INTESTINAL CELLULAR STATES IN CROHN’S DISEASE

Stefania Vetrano

Evidence of disordered eating in disorders of gut–brain interaction

Chloé Melchior

UEG Presentation

New

Share via Email Share on Facebook Share on X Share on LinkedIn Share on Bluesky

This content is part of Gutflix. Log in with your myUEG account, or create one free, to watch it.

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Ostomy management

Revital Barkan 1

Affiliations

1 Department of Gastroenterology Rabin Medical Center - Beilinson Hospital, Petah Tikva, Israel

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Abstract

Event

UEG Week Barcelona 2026

Topics

Colorectal Surgery IBD

Session

Mistakes in… Lower GI

Citation

2026: United European Gastroenterology Journal 2026; 14 (S1)

Published

2026

More Like This:

DIET QUALITY AND DIVERSITY IN CHILDHOOD AND ADOLESCENCE AND LATER RISK OF INFLAMMATORY BOWEL DISEASE: A TRI-NATIONAL BIRTH COHORT STUDY

Karl Mårild

CONSUMPTION OF ULTRA-PROCESSED FOOD PROMOTE INFLAMMATORY POTENTIAL OF FECAL MICROBIOME THROUGH ALTERING THE BALANCE OF TH17 AND RORYT TREG

Williams Turpin

FRUCTANS BOOST COLONIC FERMENTATION BUT DO NOT AGGRAVATE SYMPTOMS IN NON-CONSTIPATED IBS PATIENTS ON A LOW FODMAP DIET – A RANDOMIZED CONTROLLED TRIAL

Magnus Simrén

Ostomy management

Revital Barkan

HIGH ADHERENCE TO THE MEDITERRANEAN DIET DELAYS SURGERY AND REPROGRAMS INTESTINAL CELLULAR STATES IN CROHN’S DISEASE

Stefania Vetrano

Evidence of disordered eating in disorders of gut–brain interaction

Chloé Melchior

UEG Presentation

New

Share via Email Share on Facebook Share on X Share on LinkedIn Share on Bluesky

HIGH ADHERENCE TO THE MEDITERRANEAN DIET DELAYS SURGERY AND REPROGRAMS INTESTINAL CELLULAR STATES IN CROHN’S DISEASE

This content is part of Gutflix. Log in with your myUEG account, or create one free, to watch it.

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HIGH ADHERENCE TO THE MEDITERRANEAN DIET DELAYS SURGERY AND REPROGRAMS INTESTINAL CELLULAR STATES IN CROHN’S DISEASE

Alejandra Angela Carriles Linares 1,2, Michele Salerno 1,2, Stefano De Zanet 1,2, Faris Hrvat 1, Laura Loy 2, Roberto Gabbiadini 2, Patrizia Gnagnarella 3, Giuseppe Privitera 1,2, Arianna Dal Buono 2, Cristina Bezzio 1,2, Daniele Piovani 1,2, Stefanos Bonovas 1,2, Gisella Figlioli 1,2, Giulia Rizzo 2, Giada Mori 2, Gianluca Tognon 4, Samuel Elias Pineda Chavez 2,1, Massimo Claudio Fantini 5,6, Sara Onali 5,6, Michele Carvello 1,2, Antonino Spinelli 1,2, Alessandro Armuzzi 1,2, Stefania Vetrano 2,1

Affiliations

1 Humanitas University, Pieve Emanuele, Milan, Italy

2 IRCCS Humanitas Research Hospital, Rozzano, Milan, Italy

3 IEO European Institute of Oncology IRCCS, Milan, Italy

4 University of Skövde, Skövde, Sweden

5 Azienda Ospedaliero-Universitaria di Cagliari, Monserrato, Cagliari, Italy

6 University of Cagliari, Monserrato, Cagliari, Italy

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Abstract

Introduction

Fibrostenotic Crohn’s disease (CD) leads to intestinal obstruction and surgery, yet determinants of fibrogenesis remain poorly defined. While dietary patterns influence inflammation, their role in fibrotic progression remains unclear. We investigated whether Mediterranean diet adherence influences disease progression.

Aims & Methods

We conducted a retrospective cohort study including 1,092 patients with Crohn’s disease from two tertiary referral centers (mean age at diagnosis 33.6 years, SD 15.3; 54% male), with B1 disease in 67%, B2 in 27%, and B3 in 6%. Mediterranean diet adherence was quantified using a validated food frequency questionnaire and a 0–9-point score.
The primary outcome was intestinal surgery for fibrostenotic CD, and the secondary outcome was de novo intestinal stenosis. Time-to-event analyses were performed using Kaplan–Meier estimates and multivariable Cox regression, with time zero defined as first clinical assessment. Patients were censored at last clinical follow-up for surgery and at last colonoscopy for stenosis, reflecting routine clinical practice with variable follow-up intervals.
Mechanistic studies were performed in SAMP1/YitFc mice fed a Mediterranean or control diet for 12 weeks. Disease severity, fibrosis, and ileal remodeling were assessed. Spatial transcriptomics was performed in murine tissue, while bulk RNA sequencing was conducted on fibroblasts from 10 CD patients stratified by diet adherence.

Results

Over a median follow-up of 2.54 years (3,772 person-years), 313 patients (28.7%) underwent surgery, corresponding to an incidence rate of 8.3 per 100 person-years. The 5-year cumulative incidence of surgery decreased progressively across Mediterranean diet adherence levels (39.2% low, 31.8% moderate, 25.0% high; p < 0.001).
For de novo stenosis, the 5-year cumulative incidence was 49.6% (95% CI 45.6–53.2%), with a graded reduction across adherence levels (56.4%, 51.2%, 35.8%). Multivariable models confirmed an independent protective association between higher Mediterranean diet adherence and both outcomes.
In mice, the Mediterranean diet attenuated intestinal inflammation and collagen deposition compared with the control diet (p < 0.001).
Spatial transcriptomics revealed diet-dependent remodeling of the intestinal microenvironment, characterized by expansion of goblet cells and RGS5+ structural myofibroblasts, with reduced SPP1+ pro-fibrotic and CD74+ inflammatory fibroblasts. In contrast, the control diet promoted inflammatory and metabolically dysregulated stromal states. Similarly, in human samples, high Mediterranean diet adherence was associated with enrichment of RGS5+ structural myofibroblasts in the intestinal mucosa.

Conclusion

Higher adherence to the Mediterranean diet is associated with reduced risk of intestinal surgery and de novo stenosis in CD. Integrated human and experimental data suggest that the Mediterranean diet may modulate fibrostenotic progression by directly reshaping epithelial and stromal cellular states, beyond anti-inflammatory effects, providing a potential strategy to influence intestinal tissue remodeling.

Event

UEG Week Barcelona 2026

Topics

Paediatrics Small Intestine & Nutrition IBD Gut Microbiota

Submission format

Abstract

Session

Beyond prescriptions: Improving IBD outcomes with non-pharmaceutical approaches

Citation

2026: United European Gastroenterology Journal 2026; 14 (S1)

Published

2026

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Evidence of disordered eating in disorders of gut–brain interaction

Chloé Melchior 1

Affiliations

1 Rouen University Hospital, INSERM U1073, CIC-CRB-1404, Rouen, France

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Abstract

Event

Postgraduate Teaching Programme Barcelona 2026

Topics

Neurogastroenterology & Motility Small Intestine & Nutrition

Session

Eating disorders and unexplained weight loss

Citation

2026: United European Gastroenterology Journal 2026; 14 (S1)

Published

2026

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Karl Mårild

CONSUMPTION OF ULTRA-PROCESSED FOOD PROMOTE INFLAMMATORY POTENTIAL OF FECAL MICROBIOME THROUGH ALTERING THE BALANCE OF TH17 AND RORYT TREG

Williams Turpin

FRUCTANS BOOST COLONIC FERMENTATION BUT DO NOT AGGRAVATE SYMPTOMS IN NON-CONSTIPATED IBS PATIENTS ON A LOW FODMAP DIET – A RANDOMIZED CONTROLLED TRIAL

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HIGH ADHERENCE TO THE MEDITERRANEAN DIET DELAYS SURGERY AND REPROGRAMS INTESTINAL CELLULAR STATES IN CROHN’S DISEASE

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