PD383 - DIETARY QUALITY AND METABOLIC-HEPATIC MARKERS ACROSS OBESITY CATEGORIES IN MASLD

Linked sessions

PD383

DIETARY QUALITY AND METABOLIC-HEPATIC MARKERS ACROSS OBESITY CATEGORIES IN MASLD

M. D. M. d'Orey1, I. Matias1,*, J. Estrabocha1,2, S. Carvalhana1,3, R. Fernandes3, M. Carvalho3, A. Neves3, F. Capinha3, H. Cortez-Pinto4,5, S. Policarpo6 on behalf of The GRIPonMASH project is supported by the Innovative Health Initiative Joint Undertaking (IHI JU) under grant agreement No 101132946. The JU receives support from the European Union’s Horizon Europe research and innovation programme and COCIR, EFPIA, Eur

1Associação para Investigação e Desenvolvimento da Faculdade de Medicina, Lisboa, 2USF Sesimbra, Setúbal, 3ULS Santa Maria, Gastroenterology Service, 4Faculdade de Medicina, Clínica Universitária de Gastroenterologia, 5ULS Santa Maria, Associação para Investigação e Desenvolvimento da Faculdade de Medicina, 6Faculdade de Medicina, Nutrition Laboratory, Lisboa, Portugal

 

Rationale: Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) diagnosed by hepatic steatosis plus cardiometabolic risk factors. Dietary patterns drive disease progression, making lifestyle key in management. Characterised MASLD patients using anthropometric, biochemical and hepatic markers, exploring associations with dietary patterns.

Methods: Collected demographics, biochemical markers (HOMA-IR, HbA1c, AST, ALT), hepatic elastography (Fibroscan®: CAP, LSM) and anthropometry (BMI, waist circumference-WC and neck circumference-NC). NC cut-offs of ≥39.4cm (♂) and ≥33.7cm (♀) identified insulin resistance. Healthy Eating Index (HEI, 0-100) from the Food Frequency Questionnaire; higher scores reflect cardioprotective patterns. Patients classified as preclinical (excess adiposity+preserved organ function) or clinical obesity (excess adiposity+metabolic complications: hyperglycemia, dyslipidemia, reduced eGFR, hepatic fibrosis, hypertension or sleep apnea).

Results: 306 participants (55.6%♀; mean age 55.1), 46.9% clinical obesity and 7.9% preclinical. Most had low fibrosis risk (92.1%) and low-grade steatosis (67.6%) with: 49.7% insulin resistance, 43.7% pre-diabetes, 61.8% elevated WC and 40.5% elevated NC. Mean HEI was 55.1 (medium quality). Clinical obesity associated with higher WC, CAP and AST vs non-obese (p≤0.007). HEI scores did not differ across obesity groups (p= 0,132). Weak negative correlations were found between HEI and BMI (p=0.043), NC (p=0.002) and CAP (p=0.35).

Conclusion: Despite weak inverse correlations between dietary quality and adiposity, HEI was not independently associated with hepatic or metabolic outcomes. HOMA-IR and HbA1c were linked to fibrosis severity, reinforcing metabolic dysregulation as key MASLD driver. Clinical obesity strongly associated with hepatic steatosis and liver markers regardless of diet, stressing the need for integrated metabolic approaches beyond dietary quality alone.

Disclosure of Interest: None declared