PD472 - REGULATION OF APELIN AND ITS RECEPTOR APJ IN SKELETALMUSCLE

PD472

REGULATION OF APELIN AND ITS RECEPTOR APJ IN SKELETAL

MUSCLE

S. Weigand^1,*, S. Kaser¹, K. Salzmann¹

¹Innere Medizin I, Medizinische Universität Innsbruck, Innsbruck, Austria

Rationale: Sarcopenia is a prevalent and clinically relevant comorbidity in patients with type 2 diabetes, yet no causal pharmacological therapy exists. This study aimed to investigate whether the antidiabetic agents metformin and pioglitazone modulate sarcopenic processes via the apelin/APJ signaling pathway in skeletal muscle cells.

Methods: An in vitro model using L6 skeletal muscle cells was employed to investigate the effects of metformin and pioglitazone on the apelin/APJ signaling pathway. Cells were treated with the respective agents, and protein expression levels of apelin and its receptor APJ were analyzed by Western blot. Densitometric quantification was performed, and results were compared between treatment groups and untreated controls. Statistical analysis was conducted using one-way ANOVA, with significance defined as p < 0.05.

Results: Western blot analysis revealed no significant differences in the protein expression levels of apelin or its receptor APJ between metformin-, pioglitazone-treated, and control cells. Densitometric quantification confirmed the absence of statistically significant changes across all groups (one-way ANOVA, p ≥ 0.05).

Conclusion: The results of the study indicate that neither metformin nor pioglitazone significantly alter the protein expression of apelin or its receptor APJ in L6 myocytes. Thus, a direct influence of these antidiabetic drugs on sarcopenic processes via the apelin/APJ system could not be demonstrated in the investigated in vitro model.

For clinical practice, this implies that, given the current lack of an approved pharmacological therapy for sarcopenia, progressive resistance training and a protein-rich diet remain the most effective measures for prevention and treatment. Future research is required to investigate potential systemic effects or other signaling pathways that extend beyond the isolated cell model.

Disclosure of Interest: None declared