# Multi-Omics Analysis of Morbid Obesity Using a Patented Unsupervised Machine Learning Platform: Genomic, Biochemical, and Glycan Insights

**Authors:** Irena Šnajdar, Luka Bulić, Andrea Skelin, Leo Mršić, Mateo Sokač, Maja Brkljačić, Martina Matovinović, Martina Linarić, Jelena Kovačić, Petar Brlek, Gordan Lauc, Martina Smolić, Dragan Primorac

PMC · DOI: 10.3390/ijms27031551 · International Journal of Molecular Sciences · 2026-02-04

## TL;DR

This study uses AI and multi-omics data to develop personalized diets for morbid obesity, successfully reducing BMI and biological age markers.

## Contribution

A patented AI platform is used to stratify patients and generate personalized dietary recommendations based on multi-omics data.

## Key findings

- Personalized nutrigenetic dietary interventions significantly reduced BMI and GlycanAge index in morbidly obese patients.
- Patients exhibited accelerated biological aging, as indicated by elevated GlycanAge compared to chronological age.
- AI clustering identified a uniform genetic profile among patients with morbid obesity.

## Abstract

Morbid obesity is a complex, multifactorial disorder characterized by metabolic and inflammatory dysregulation. The aim of this study was to observe changes in obese patients adhering to a personalized nutrition plan based on multi-omic data. This study included 14 adult patients with a body mass index (BMI) > 40 kg/m2 who were consecutively recruited from those presenting to our outpatient clinic and who met the inclusion criteria. Clinical, biochemical, hormonal, and glycomic parameters were assessed, along with whole-genome sequencing (WGS) that included a focused analysis of obesity-associated genes and an extended analysis encompassing genes related to cardiometabolic disorders, hereditary cancer risk, and nutrigenetic profiles. Patients were stratified into nutrigenetic clusters using a patented unsupervised machine learning platform (German Patent Office, No. DE 20 2025 101 197 U1), which was employed to generate personalized nutrigenetic dietary recommendations for patients with morbid obesity to follow over a six-month period. At baseline, participants exhibited elevated glucose, insulin, homeostatic model assessment for insulin resistance (HOMA-IR), triglycerides, and C-reactive protein (CRP) levels, consistent with insulin resistance and chronic low-grade inflammation. The majority of participants harbored risk alleles within the fat mass and obesity-associated gene (FTO) and the interleukin-6 gene (IL-6), together with multiple additional significant variants identified across more than 40 genes implicated in metabolic regulation and nutritional status. Using an AI-driven clustering model, these genetic polymorphisms delineated a uniform cluster of patients with morbid obesity. The mean GlycanAge index (56 ± 12.45 years) substantially exceeded chronological age (32 ± 9.62 years), indicating accelerated biological aging. Following a six-month personalized nutrigenetic dietary intervention, significant reductions were observed in both BMI (from 52.09 ± 7.41 to 34.6 ± 9.06 kg/m2, p < 0.01) and GlycanAge index (from 56 ± 12.45 to 48 ± 14.83 years, p < 0.01). Morbid obesity is characterized by a pro-inflammatory and metabolically adverse molecular signature reflected in accelerated glycomic aging. Personalized nutrigenetic dietary interventions, derived from AI-driven analysis of whole-genome sequencing (WGS) data, effectively reduced both BMI and biological age markers, supporting integrative multi-omics and machine learning approaches as promising tools in precision-based obesity management.

## Linked entities

- **Genes:** FTO (FTO alpha-ketoglutarate dependent dioxygenase) [NCBI Gene 79068], IL6 (interleukin 6) [NCBI Gene 3569]
- **Diseases:** morbid obesity (MONDO:0005139)

## Full-text entities

- **Genes:** IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}
- **Diseases:** obese (MESH:D009765), cancer (MESH:D009369), cardiometabolic disorders (MESH:D024821), insulin resistance (MESH:D007333), inflammatory dysregulation (MESH:D021081), Morbid Obesity (MESH:D009767), fat (MESH:D004620), inflammation (MESH:D007249)
- **Chemicals:** glucose (MESH:D005947), triglycerides (MESH:D014280)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12898758/full.md

## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12898758/full.md

## References

30 references — full list in the complete paper: https://tomesphere.com/paper/PMC12898758/full.md

---
Source: https://tomesphere.com/paper/PMC12898758