9th International congress of the Molecular Biology Association of Turkey, İzmir, Türkiye, 12 - 14 Eylül 2024, cilt.9, sa.2024, ss.1015, (Özet Bildiri)
Background/Aim: Diabetic cardiomyopathy is a
structural and functional myocardial disorder associated with diabetes that is
not associated with the traditional factors. In the healthy heart, glucose and
long-chain fatty acids are used equally as energy sources. There is a dynamic
balance in their uptake and transport. Adiponectin (APN) is an adipokine
synthesized and secreted by adipose tissue. APN concentration is reduced in
insulin resistance and type 2 diabetes. APN prevents insulin resistance by
increasing fatty acid excretion and glucose by skeletal muscle. CD36 plays a
role in lipid metabolism and signal transduction. It facilitates the cellular
uptake of LCFA in the plasma membrane, especially in the heart and skeletal
muscles. Blocking CD36 in cardiomyocytes results in the prevention of excessive
lipid uptake.The aim of this study is to search the effect of adiponectin on
changes in gene expression responsible for fatty acid uptake and transport in
cardiac cell in vitro.
Materials and Methods: Immunofluorescence (IF)
staining was performed with demonstrated primary and secondary antibodies for
cardiac-specific myosin, muscle-specific desmin intermediate filaments, and
specific granules containing perinuclear Atrial Natriuretic Factor (ANF) to
demonstrate cardiac behaviour of H9c2 cell line. H9c2 cardiac in vitro
cell model that mimicking diabetic cardiomyopathy was created and the effect of
adiponectin on the expression changes of CD36 gene under basal, hypoglycemic
and hyperglycemic conditions was determined by Western blot.
Results: In the IF study showed H9c2 cell line’s
cardiac behavior. Time-dependent treatment of APN in different concentrations
to H9c2 cells resulted in changes in CD36 expression. From this, it can be
suggested that APN may be effective in fatty acid translocation.
Conclusion: This study aims to define new mechanisms
that play a role in the pathogenesis of Diabetic cardiomyopathy.