# Autotaxin and Lysophosphatidic Acid Circulating Levels Correlate with Body Mass Index in Obese Subjects with MASLD

## TL;DR

This study found that autotaxin levels increase with BMI in obese individuals with MASLD, while lysophosphatidic acid levels decrease, suggesting a link to metabolic and inflammatory changes.

## Contribution

The study reveals a novel association between autotaxin and BMI in MASLD patients, indicating a potential role in obesity-related metabolic alterations.

## Key findings

- Autotaxin levels positively correlate with BMI in MASLD patients.
- Lysophosphatidic acid levels negatively correlate with BMI and its interaction with ATX.
- Higher autotaxin concentrations were observed in obese females compared to males.

## Abstract

Scientific evidence supports the role of the autotaxin-lysophosphatidic acid (ATX-LPA) pathway in obesity and liver damage. The present study aim is to investigate variations in serum ATX and LPA levels across different BMI categories in a subcohort of subjects with MASLD. The study sample comprises 199 patients with liver steatosis from the most recent follow-up of the MICOL study, a prospective cohort study established in 1985, based on a random sample of the population of Castellana Grotte. In adjusted model, a positive association of BMI with ATX was observed when modeled as both a continuous (β = 0.018, p < 0.001, 0.012 to 0.024 95% C.I.) and categorical variable β = 0.170, p < 0.001, 0.111 to 0.228 95% C.I.). Conversely, a negative association was observed for LPA alone (β = −0.083, p = 0.020, −0.152 to −0.013 95% C.I.) and for the BMI and LPA interaction term (β = −0.109, p = 0.002, −0.176 to −0.042 95% C.I.). A positive association between ATX levels and BMI was found, whereas LPA levels tended to decrease with increasing BMI. Within the obese subgroup, ATX concentrations were notably higher in female compared to male participants. These findings suggest that elevated ATX in MASLD may reflect obesity-related metabolic and inflammatory alterations rather than adiposity alone, possibly involving altered LPA feedback and metabolism.