PP209 - INSULIN RESISTANCE AND RESPONSE TO NUTRITIONAL THERAPY: A SECONDARY ANALYSIS OF THE RANDOMIZED EFFORT TRIAL

PP209

INSULIN RESISTANCE AND RESPONSE TO NUTRITIONAL THERAPY: A SECONDARY ANALYSIS OF THE RANDOMIZED EFFORT TRIAL

C. Wunderle^1,*, P. Mamot^1,2, V. Haller^1,3, P. Tribolet^1,4,5, Z. Stanga⁶, B. Müller^1,2, P. Schütz^1,2

¹Medical University Clinic, Cantonal Hospital Aarau, Aarau, ²Medical Faculty, University of Basel, Basel, Switzerland, ³Department of Nutritional Science, Justus Liebig University, Giessen, Germany, ⁴Department of Health Professions, Bern University of Applied Sciences, Bern, Switzerland, ⁵Faculty of Life Sciences , University of Vienna, Vienna, Austria, ⁶Division of Diabetes, Endocrinology, Nutritional Medicine, and Metabolism, Bern University Hospital and University of Bern, Bern, Switzerland

Rationale: Understanding differences in patients’ metabolic phenotypes and how these influence responses to nutritional interventions has become an important area of research. Among participants in the Effect of Early Nutritional Therapy on Frailty, Functional Outcomes, and Recovery of Malnourished Medical Inpatients (EFFORT) trial, we analyzed metabolic markers associated with glucose and stress metabolism to explore their potential to predict clinical risk and response to nutritional therapy.

Methods: In this secondary analysis of the multicenter, randomized-controlled EFFORT trial, we phenotyped patients according to their Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) calculated from fasting insulin and glucose levels at hospital admission using biobank samples. We calculated Cox models adjusted for sex, randomization, malnutrition risk severity and cancer diagnosis. The primary endpoint was 30-day all-cause mortality.

Results: We included 997 patients with complete biomarker information, 24% of whom had elevated insulin levels. High fasting insulin levels were associated with better 30-day survival (adj. HR for 30-day mortality 0.44, 95% CI 0.20 to 0.97), p=0.04). Compared to patients with lower levels, patients with high fasting insulin levels as well as patients with high HOMA-IR levels showed a pronounced benefit from the nutritional intervention (HR 0.15 and 0.10, p-value for interaction with insulin as an effect modifier 0.13 and with HOMA-IR 0.30).

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Conclusion: This analysis suggests that among medical patients at nutritional risk, elevated insulin resistance, reflected by higher HOMA-IR and/or fasting insulin levels, may indicate a favorable response to nutritional interventions. Further research into the metabolic pathways underlying these findings is warranted to advance patient phenotyping based on metabolic profiles and to guide personalized nutritional strategies.

Disclosure of Interest: C. Wunderle Other: CW reports a relationship with Nestlé Health Science, Nutricia Danone, BBraun, Baxter, Abbott Nutrition that includes: lecture fee., P. Mamot: None declared, V. Haller: None declared, P. Tribolet Other: PT reports a relationship with Nestlé Health Science and Abbott Nutrition that includes: lecture fee., Z. Stanga Grant / Research Support from: ZS reports a relationship with Nestlé Health Science, Fresenius Kabi and B. Braun that includes: funding grants. , B. Müller: None declared, P. Schütz Grant / Research Support from: PS reports a relationship with Roche, Thermo Fisher, bioMérieux, Nestlé Health Science and Abbott Nutrition that includes: funding grants.