Phosphatidylinositol 4-kinase IIIβ mediates contraction-induced GLUT4 translocation and shows its anti-diabetic action in cardiomyocytes.

ABSTRACT: In the diabetic heart, long-chain fatty acid (LCFA) uptake is increased at the expense of glucose uptake. This metabolic shift ultimately leads to insulin resistance and a reduced cardiac function. Therefore, signaling kinases that mediate glucose uptake without simultaneously stimulating LCFA uptake could be considered attractive anti-diabetic targets. Phosphatidylinositol-4-kinase-IIIβ (PI4KIIIβ) is a lipid kinase downstream of protein kinase D1 (PKD1) that mediates Golgi-to-plasma membrane vesicular trafficking in HeLa-cells. In this study, we evaluated whether PI4KIIIβ is involved in myocellular GLUT4 translocation induced by contraction or oligomycin (an F₁F₀-ATP synthase inhibitor that activates contraction-like signaling). Pharmacological targeting, with compou

SUBMITTER: Sun A 

PROVIDER: S-EPMC8004495 | biostudies-literature | 2021 Mar

REPOSITORIES: biostudies-literature