# Association between different metabolic obesity phenotypes and colorectal adenoma

**Authors:** Li Lin, Yuhan Ying, Long Shu, Xiaoling Lv, Qin Zhu, Miquel Vall-llosera Camps, Muhammad Shahzad Aslam, Muhammad Shahzad Aslam, Muhammad Shahzad Aslam

PMC · DOI: 10.1371/journal.pone.0343556 · PLOS One · 2026-02-23

## TL;DR

This study finds that metabolically unhealthy obesity types are linked to higher colorectal adenoma risk, especially in certain age and sex groups.

## Contribution

The study introduces a classification of obesity phenotypes based on metabolic status and BMI to assess colorectal adenoma risk.

## Key findings

- Metabolically unhealthy non-obesity and obesity are significantly linked to higher colorectal adenoma risk.
- Risk is more pronounced in women with metabolically unhealthy non-obesity and in older individuals with metabolically unhealthy obesity.
- Metabolically healthy obesity does not show increased risk compared to metabolically healthy non-obesity.

## Abstract

Obesity and metabolic abnormalities are independently and interactively associated with colorectal adenoma (CRA). This study aimed to investigate the association between different metabolic obesity phenotypes and CRA, and to assess whether this relationship is influenced by stratification based on age and sex.

A total of 2042 subjects were enrolled in this study. The patients were classified into four metabolic obesity phenotypes based on their body mass index (BMI) and metabolic status, including metabolically healthy non-obesity (MHNO), metabolically unhealthy non-obesity (MUNO), metabolically healthy obesity (MHO), and metabolically unhealthy obesity (MUO). Multiple logistic regression analysis and further subgroup analysis based on sex and age were performed to evaluate the association between the metabolic obesity phenotypes and the occurrence of CRA.

In the overall population, CRA was detected at significantly higher rates in both the MUNO and MUO phenotypes compared to the MHNO and MHO phenotypes. After adjusting for confounders, in the overall population, the MUNO (OR = 1.353, 95% CI: 1.099–1.666, P < 0.05) and MUO (OR = 1.558, 95% CI: 1.111–2.187, P < 0.05) phenotypes were identified as risk factors for the development of CRA compared to the MHNO phenotype. Subgroup analysis based on sex revealed that in female subjects, the MUNO phenotype (OR 1.694; 95% CI 1.243–3.308, p < 0.01) exhibited significantly elevated risks of CRA compared to those in the MHNO phenotype, whereas the MHO phenotype showed no significant differences. Furthermore, in the male subjects, no statistically significant differences were observed among the four groups. Subgroup analysis based on age revealed that under 60 years with the MUNO (OR = 1.648, 95% CI: 1.252–2.169, P < 0.01) phenotype and over 60 years with MUO (OR = 2.301, 95% CI: 1.252–4.348, P < 0.01) phenotype, had significantly increased risks of CRA.

Metabolically unhealthy phenotypes are associated with a higher risk of CRA incidence. Clinical screening for CRA should focus on metabolically unhealthy subjects.

## Linked entities

- **Diseases:** colorectal adenoma (MONDO:0005484)

## Full-text entities

- **Genes:** Ren (renin) [NCBI Gene 24715] {aka RATRENAA, RENAA, Ren1}, MTMR11 (myotubularin related protein 11) [NCBI Gene 10903] {aka CRA}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, IGF1 (insulin like growth factor 1) [NCBI Gene 3479] {aka IGF, IGF-I, IGFI, MGF}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, ASPRV1 (aspartic peptidase retroviral like 1) [NCBI Gene 151516] {aka ADLI, MUNO, SASP, SASPase, Taps}, LEP (leptin) [NCBI Gene 3952] {aka LEPD, OB, OBS}
- **Diseases:** metabolic abnormalities (MESH:D008659), esophagitis (MESH:D004941), visceral adiposity (MESH:D007418), colorectal polyps (MESH:D003111), Obese (MESH:D009765), organ failure (MESH:D009102), CRA (MESH:D000236), overweight (MESH:D050177), benign tumor (MESH:D009369), diabetes (MESH:D003920), dysbiosis (MESH:D064806), rectal adenomas (MESH:D012002), ORCID iD (MESH:C535742), colonic mucosal inflammation (MESH:D007249), dysmetabolism (MESH:D024821), Hyperglycemia (MESH:D006943), prostate cancer (MESH:D011471), Dyslipidemia (MESH:D050171), MHNO (MESH:D000067329), HIV infection (MESH:D015658), lipid abnormalities (MESH:D011017), intestinal lesions (MESH:D007410), ulcerative colitis (MESH:D003093), colonic preneoplastic lesions (MESH:D003108), Type 2 Diabetes (MESH:D003924), inflammatory bowel illness (MESH:D015212), polyps (MESH:D011127), gastrointestinal cancer (MESH:D005770), cardiovascular diseases (MESH:D002318), Crohn's disease (MESH:D003424), gastrointestinal polys (MESH:D005767), familial adenomatous polyposis (MESH:D011125), insulin resistance (MESH:D007333), precancerous lesion (MESH:D011230), hyperinsulinemia (MESH:D006946), hypertension (MESH:D006973), hyperglycemic (MESH:D006944), CRC (MESH:D015179)
- **Chemicals:** cholesterol (MESH:D002784), 17 beta-estradiol (MESH:D004958), polyethylene glycol (MESH:D011092), aldosterone (MESH:D000450), simple sugars (MESH:D009005), triglyceride (MESH:D014280), azoxymethane (MESH:D001397), Alcohol (MESH:D000438), glucose (MESH:D005947), lipid (MESH:D008055), lipopolysaccharides (MESH:D008070), carbohydrate (MESH:D002241), MHNO (-), bile acid (MESH:D001647), TG (MESH:D013866)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Rattus norvegicus (brown rat, species) [taxon 10116], 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/PMC12928563/full.md

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12928563/full.md

## References

47 references — full list in the complete paper: https://tomesphere.com/paper/PMC12928563/full.md

---
Source: https://tomesphere.com/paper/PMC12928563