# Precision Medicine in Inflammatory Bowel Disease: The Emerging Role of Metabolic Dysfunction

**Authors:** Aditya Kotha, Arun J. Sanyal, Raseen Tariq

PMC · DOI: 10.3390/jpm16030139 · 2026-03-02

## TL;DR

This paper explores how metabolic issues like obesity and liver disease affect inflammatory bowel disease and how this knowledge can improve personalized treatment.

## Contribution

The paper highlights how metabolic dysfunction is a clinically meaningful factor in IBD, offering new insights for precision medicine.

## Key findings

- Metabolic comorbidities influence IBD disease course and outcomes.
- Metabolic assessment can improve personalized IBD management.
- Metabolic factors complement traditional inflammatory markers in monitoring IBD.

## Abstract

Inflammatory bowel disease (IBD), encompassing ulcerative colitis (UC) and Crohn’s disease (CD), is a chronic inflammatory disorder of the gastrointestinal tract with a rapidly increasing global prevalence. In parallel, metabolic comorbidities including obesity, metabolic dysfunction-associated steatotic liver disease (MASLD), and sarcopenia are becoming increasingly common among patients with IBD and are now recognized as important modifiers of disease course and outcomes. As the therapeutic landscape of IBD continues to evolve, these intersecting trends create an opportunity to advance precision medicine through more individualized approaches to care. This review synthesizes established and emerging evidence on the role of metabolic dysfunction in IBD, focusing on epidemiology, risk factors, and prognostic implications. We highlight key domains relevant to personalized care, including metabolic phenotypes, energy metabolism, circulating biomarkers, and nutrition, and discuss how these factors may complement traditional inflammatory markers in risk stratification and longitudinal disease monitoring. Collectively, the available evidence suggests that metabolic comorbidities are not merely coincidental but represent clinically meaningful phenotypes that influence treatment response, complications, and long-term outcomes in IBD. Integrating metabolic assessment into routine IBD care may enable more precise, patient-centered management strategies and help address the growing heterogeneity of IBD in the era of precision medicine.

## Linked entities

- **Diseases:** inflammatory bowel disease (MONDO:0005265), ulcerative colitis (MONDO:0005101), Crohn’s disease (MONDO:0005011), obesity (MONDO:0011122), metabolic dysfunction-associated steatotic liver disease (MONDO:0013209)

## Full-text entities

- **Genes:** INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, GLP1R (glucagon like peptide 1 receptor) [NCBI Gene 2740] {aka GLP-1, GLP-1-R, GLP-1R}, LEP (leptin) [NCBI Gene 3952] {aka LEPD, OB, OBS}, IFNG (interferon gamma) [NCBI Gene 3458] {aka IFG, IFI, IMD69}, MSTN (myostatin) [NCBI Gene 2660] {aka GDF8, MSLHP}, RETN (resistin) [NCBI Gene 56729] {aka ADSF, FIZZ3, RENT, RETN1, RSTN, XCP1}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, ADIPOQ (adiponectin, C1Q and collagen domain containing) [NCBI Gene 9370] {aka ACDC, ACRP30, ADIPQTL1, ADPN, APM-1, APM1}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, MBTPS1 (membrane bound transcription factor peptidase, site 1) [NCBI Gene 8720] {aka CAOP, PCSK8, S1P, SEDKF, SKI-1}
- **Diseases:** colitis (MESH:D003092), enteric nutrient loss (MESH:D004751), fatigue (MESH:D005221), lean (MESH:D013851), Metabolic Syndrome (MESH:D024821), liver injury (MESH:D017093), heart failure (MESH:D006333), muscle (MESH:D019042), MASLD (MESH:D008107), glucose intolerance (MESH:D018149), immune-metabolic disorder (MESH:D007154), cardiovascular disease (MESH:D002318), hypertension (MESH:D006973), immune dysregulation (OMIM:614878), gut dysbiosis (MESH:D064806), systemic (MESH:D015619), adipose dysfunction (MESH:D018205), inflammatory cytokines (MESH:D000080424), hepatic steatosis (MESH:D005234), Intestinal inflammation (MESH:D007249), thrombotic (MESH:D013927), gastrointestinal disease (MESH:D005767), atherogenic (MESH:D050197), choline deficiency (MESH:D002796), Deficiencies (MESH:D007153), ischemic heart disease (MESH:D017202), visceral adiposity (MESH:D007418), liver cirrhosis (MESH:D008103), Metabolic Dysfunction (MESH:D008659), injury to (MESH:D014947), hepatic disease (MESH:D056486), infection (MESH:D007239), Insulin Resistance (MESH:D007333), IBS (MESH:D053560), muscle loss (MESH:D009135), stroke (MESH:D020521), Composition (MESH:D058617), atherogenic dyslipidemia (MESH:D050171), metabolic dysregulation (MESH:D021081), malabsorption (MESH:D008286), IBD (MESH:D015212), UC (MESH:D003093), diminished quality of life (MESH:D003643), fibrosis (MESH:D005355), Malnutrition (MESH:D044342), abnormal body composition (MESH:C564221), endotoxemia (MESH:D019446), inflamed (MESH:C531841), cancer (MESH:D009369), weight loss (MESH:D015431), NAFLD (MESH:D065626), CD (MESH:D003424), Obesity (MESH:D009765), type 2 diabetes (MESH:D003924), atrophy (MESH:D001284), chronic illness (MESH:D002908), Sarcopenia (MESH:D055948), impaired glucose regulation (MESH:C565631), overweight (MESH:D050177)
- **Chemicals:** lipopolysaccharide (MESH:D008070), sphingomyelin (MESH:D013109), vitamin D. (MESH:D014807), carbohydrate (MESH:D002241), iron (MESH:D007501), sphingosine (MESH:D013110), sucrose (MESH:D013395), vitamin B12 (MESH:D014805), Lipid (MESH:D008055), glucose (MESH:D005947), Butyrate (MESH:D002087), fats (MESH:D005223), starches (MESH:D013213), triglycerides (MESH:D014280), sugar (MESH:D000073893), zinc (MESH:D015032), Short-chain fatty acids (MESH:D005232), folic acid (MESH:D005492), BioRender (-), sphingosine-1-phosphate (MESH:C060506), magnesium (MESH:D008274), ceramide (MESH:D002518), Oxylipins (MESH:D054883), bile acid (MESH:D001647), fructose (MESH:D005632), leucine (MESH:D007930), Endocannabinoids (MESH:D063388), Sphingolipids (MESH:D013107), olive oil (MESH:D000069463), anandamide (MESH:C078814)
- **Species:** Homo sapiens (human, species) [taxon 9606], Mus musculus (house mouse, species) [taxon 10090]

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13027519/full.md

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Source: https://tomesphere.com/paper/PMC13027519