Research Information System
X.International Congress of Molecular Medicine, İzmir, Turkey, 23 - 27 September 2024, pp.110, (Summary Text)
Diabetic
Cardiomyopathy (DCM) refers to abnormalities in the structure and function of
the myocardium resulting from diabetes. In a healthy heart, there is a balance
between the use of fatty acids and glucose as energy sources. In the presence
of DCM, the intake of long-chain fatty acids increases in a way that disrupts
this balance. CD36 facilitates the uptake of long-chain fatty acids at the
plasma membrane in the heart and skeletal muscles. The most significant process
leading to the development of cardiomyopathy is the increased uptake of fatty
acids via the CD36 pathway. GLUT4 is a glucose transporter that mediates the
uptake of glucose into the heart. AMP-activated protein kinase (AMPK), which is
activated by AMP, is responsible for the contraction-induced translocation of
CD36 and is important for the contraction-induced translocation of GLUT4. The
activation of AMPK non-selectively stimulates both glucose and long-chain fatty
acid uptake. Adiponectin is a hormone that can be found at high levels in plasma
and enhances insulin sensitivity. In rats with adiponectin resistance, the
phosphorylation processes of insulin signaling pathway proteins are disrupted,
and GLUT4 translocation is inhibited. The aim of this study is to determine the
effect of adiponectin on the disease by examining the changes in AMPK synthesis
in in vitro cardiac cell models mimicking DCM following treatment with
adiponectin. The cardiac characteristics of H9c2 cells were confirmed through
immunohistochemical staining, followed by fluorescence microscopy imaging of
muscle-specific desmin intermediate filaments, cardiac-specific myosin, and
perinuclear Atrial Natriuretic Factor (ANF). DCM model was created using the
H9c2 cell line, and Time course experiment were made with diiferent
concentration level of adiponectin at 30 minute and 1 hour to examine the
expression change of AMPK by Western
Blot method.