Free fatty acid can induce cardiac dysfunction and alter insulin signaling pathways in the heart

• DOI: 10.1186/s12944-018-0834-1
• Publication Date: 2018-08-08T13:19:36Z
• Authors: Lina Han; Jiali Liu; Leilei Zhu; Fang Tan; Yupei Qin; He Huang; Yerong Yu
• Keywords: GLUT4

Insulin resistance has been independently related to heart failure. However, the specific mechanisms of high FFA levels in pathophysiology failure insulin-resistant states are remain largely unclear. This study investigated whether elevated circulating free fatty acids (FFA) result impaired cardiac structure and function vivo via insulin-related signaling pathways myocardium. Male Wistar rats were randomly divided into intralipid group (20% plus heparin infusion) control (glycerol infusion). Blood samples collected before after 6-, 12-, 24-h infusions. Cardiac measured using echocardiography. Maximum velocity myocardial contraction (+dP/dt max) diastole (−dP/dt a physiological polygraph vivo. Heart tissues for western blotting. Compared with group, plasma FFA, glucose, serum insulin increased significantly group. With increasing infusion time, decreased gradually compared After infusion, early (E’, cm/s) diastolic peak velocities significantly. Protein expression phosphatidylinositol 3-kinase (PI3K), serine/threonine kinase Akt, phosphorylated Akt myocardium 6-h glucose transporter type 4 (GLUT4), Adenosine 5′-monophosphate -activated protein (AMPK), AMPK(p-AMPK), endothelial nitric oxide synthase (eNOS) Elevated may impair dysfunction might from significant changes PI3K-Akt-GLUT4 AMPK-eNOS levels.