Skip to main content

Advertisement

Fig. 5 | Cardiovascular Diabetology

Fig. 5

From: GLP-1 analog liraglutide-induced cardiac dysfunction due to energetic starvation in heart failure with non-diabetic dilated cardiomyopathy

Fig. 5

Protein expression and ATP content in the heart muscles of hamsters. a Liraglutide administration further upregulated cleaved caspase-3, an apoptosis marker in J2K hamsters. b Liraglutide also increased LC3 II/I level that indicated increased autophagy, suggesting that substrate starvation for cardiac muscles occurred in the liraglutide groups. c, d Liraglutide increased the levels of the glucose transporter GLUT-4 and fatty acid transporter CD36 in cardiac muscles. e The upregulation of AMPK phosphorylation tended to occur in the HF groups. f, g The ATP content in the cardiac tissues slightly decreased in the HF-H groups in 1 g cardiac muscles; however, as a whole heart, higher ATP content was estimated due to the enlarged cardiac tissue in the HF groups. *p < 0.05 vs. HF + PBS group (n = 6 in each group)

Back to article page