Vascular endothelial growth factor B inhibits lipid accumulation in C2C12 myotubes incubated with fatty acids. (4th March 2019)

• Record Type: Journal Article
• Authors: Li, Ling-Jie; Ma, Jin; Li, Song-Bo; Chen, Xuefei; Zhang, Jing
• Is Part Of: Growth factors. Volume 37:Number 1/2(2019)
• Page Start: 76
• Page End: 84
• Publication Date: 2019-03-04
• Subjects: VEGFB -- lipid accumulation -- C2C12 -- fatty acid; Growth factors -- Periodicals; Physiology -- Periodicals; 611
• DOI: 10.1080/08977194.2019.1626851
• Languages: English
• ISSNs: 0897-7194

Abstract

Abstract: To investigate (1) the effect of vascular endothelial growth factor B (VEGFB) on lipid accumulation and the alteration of fatty acids and fatty acid-related enzymes in C2C12 myotubes incubated with fatty acids and (2) the regulatory effect of VEGFB on skeletal muscle lipid metabolism. Mouse C2C12 myotubes were incubated with oleic acid (OA) and palmitic acid (PA), and differentiated mature C2C12 myotubes were treated with VEGFB. Oil-red O staining, BODIPY staining and cell triglycerides (TG) content were examined. Total RNA was isolated, and real-time PCR analysis was performed. Treatment with 100 μM OA and 50 μM PA induced lipid droplet accumulation and increased TG content ( p < .01), and 100 ng/mL VEGFB reduced lipid droplet accumulation and decreased TG content ( p < .01). Treatment with 100 ng/mL VEGFB significantly induced the mRNA expression of fatty acid transport protein 1 (FATP1) ( p < .01) and FATP4 ( p < .01). Treatment with 100 ng/mL VEGFB significantly induced the mRNA expression of adipose TG lipase and hormone-sensitive lipase ( p < .01) as well as carnitine palmitoyltransferase I ( p < .01), peroxisome proliferator-activated receptor-γ coactivator-1α ( p < .01), acyl-coa dehydrogenase very long chain ( p < .05), acyl-coa synthetase long-chain family member 1 ( p < .01), peroxisomal acyl-coenzyme A oxidase 1 ( p < .05), and mitochondrial uncoupling protein 3 ( p < .01). VEGFB enhanced FATP1and FATP4 expression, promoted C2C12 myotube fatty acid oxidation and TG decomposition, and inhibited C2C12 myotube fatty acid re-esterification, thus inhibiting lipid accumulation in C2C12 myotubes incubated with fatty acids.