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Vascular endothelial growth factor B inhibits lipid accumulation in C2C12 myotubes incubated with fatty acids.
Growth Factors ( IF 1.8 ) Pub Date : 2019-06-19 , DOI: 10.1080/08977194.2019.1626851
Ling-Jie Li 1 , Jin Ma 1 , Song-Bo Li 2 , Xuefei Chen 1 , Jing Zhang 1
Affiliation  

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.

中文翻译:

血管内皮生长因子B抑制脂质与脂肪酸一起孵育的C2C12肌管中的脂质蓄积。

研究(1)血管内皮生长因子B(VEGFB)对脂肪酸孵育的C2C12肌管中脂质积累以及脂肪酸和脂肪酸相关酶变化的影响,以及(2)VEGFB对骨骼肌的调节作用脂质代谢。将小鼠C2C12肌管与油酸(OA)和棕榈酸(PA)孵育,并用VEGFB处理分化成熟的C2C12肌管。检查了油红色O染色,BODIPY染色和甘油三酸酯(TG)含量。分离总RNA,并进行实时PCR分析。用100μMOA和50μMPA进行处理可引起脂质液滴积聚并增加TG含量(p <.01),而100 ng / mL VEGFB可减少脂质液滴积聚并降低TG含量(p <.01)。用100 ng / mL VEGFB处理可显着诱导脂肪酸转运蛋白1(FATP1)(P <.01)和FATP4(p <.01)的mRNA表达。用100 ng / mL VEGFB处理可显着诱导脂肪TG脂肪酶和激素敏感脂肪酶的mRNA表达(p <.01)以及肉碱棕榈酰转移酶I(p <.01),过氧化物酶体增殖物激活的受体-γcoactivator-1α (p <.01),超长链酰基可可脱氢酶(p <.05),酰基可可合成酶长链家族成员1(p <.01),过氧化物酶体酰基辅酶A氧化酶1(p <.05 )和线粒体解偶联蛋白3(p <.01)。VEGFB增强FATP1和FATP4表达,促进C2C12肌管脂肪酸氧化和TG分解,并抑制C2C12肌管脂肪酸再酯化,
更新日期:2019-11-01
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