Limited preventive effects of empagliflozin against metabolic dysfunction-associated steatotic liver disease in a mouse model of fast food diet

Evangelia Makri; Konstantinos Xanthopoulos; Spyros Pettas; Antonis Goulas; Panagiotis Mavrommatis-Parasidis; Eleftheria Makri; Anastasia Tsingotjidou; Angeliki Cheva; Charikleia Ntenti; Constantinos Zacharis; Iris Ballaouri; Spyridon Gerou; Stergios Polyzos

doi:10.1530/endoabs.110.P747

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Endocrine Abstracts (2025) 110 P747 | DOI: 10.1530/endoabs.110.P747

ECEESPE2025 Poster Presentations MTEabolism, Nutrition and Obesity (125 abstracts)

Limited preventive effects of empagliflozin against metabolic dysfunction-associated steatotic liver disease in a mouse model of fast food diet

Evangelia Makri ¹ , Konstantinos Xanthopoulos ¹ , Spyros Pettas ¹ , Antonis Goulas ¹ , Panagiotis Mavrommatis-Parasidis ¹ , Eleftheria Makri ¹ , Anastasia Tsingotjidou ¹ , Angeliki Cheva ¹ , Charikleia Ntenti ¹ , Constantinos Zacharis ¹ , Iris Ballaouri ² , Spyridon Gerou ² & Stergios Polyzos ¹

Author affiliations

¹Aristotle University of Thessaloniki, Thessaloniki, Greece; ²Analysis Laboratories, Thessaloniki, Greece

JOINT392

Purpose: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a highly prevalent disease with limited treatment options. The aim of this study was to evaluate the preventive effects of a sodium-glucose co-transporter (SGLT)-2 inhibitor, empagliflozin, on a dietary mouse model of MASLD.

Methods: 24 C57BL/6J mice of both sexes were randomly allocated to three groups, as follows: the fast food diet (FFD) group (eight mice, receiving a high-fat, high-cholesterol, high-fructose diet, FFD), the EMPA group (eight mice, fed a FFD with 10mg/kg/d empagliflozin), and the chow diet (eight mice, CD) group. The mice were weighed and blood samples were drawn every 4 weeks; after 25 weeks the mice were euthanized, at which point liver tissues were histologically evaluated.

Results: After 25 weeks, there was no significant difference in body weight between the three groups, whereas liver-to-body weight ratio was greater in the EMPA compared to the CD group (P = 0.002). Hepatic fibrosis was marginally different between the three groups (P = 0.045). Fibrosis stage 1 was present in five mice in FFD (62.5%), in one mouse in EMPA (12.5%), and in one mouse in CD (12.5%) group. Lipogenic, inflammatory, and fibrogenic genes did not differ between the EMPA and FFD groups. Interestingly, mRNA encoding for SGLT-1 and SGLT-2 was detected in the mouse livers.

Conclusion: Empagliflozin treatment in mice on a FFD did not result in any significant effects on morphological, biochemical, or histological features or on expression of hepatic genes associated with MASLD compared to those fed a FFD without empagliflozin. The observed effects on mild hepatic fibrosis warrant validation, possibly via studies of longer duration.