Naruta E E, Egorov A I, Omel'ianchik C N, Buko V U
Vopr Pitan. 2004;73(4):3-7.
Alimentary obesity induced by the long-term feeding of rats by high-fat diet results the reducing of rate and efficiency of oxidative phosphorylation in liver mitochondria when NAD-dependent substrates are used. The treatment of the obese rats with panthotenic acid derivatives (phosphopantotenate, panthetin, panthenol) enhanced oxidative phosphorylation of pyruvate and fatty acid carnitine esters. Among investigated compounds panthenol activated respiratory control and phosphorylation rate more effectively. Moreover, panthenol, but not phosphopanthotenate nor panthetine, increased the activity of carnitine palmitoyltransferase 1 that confirms the preferable usage of fatty acids for mitochondrial oxidation under the influence of this compound.
长期用高脂饮食喂养大鼠所诱导的营养性肥胖,会导致在使用依赖烟酰胺腺嘌呤二核苷酸(NAD)的底物时,肝脏线粒体中氧化磷酸化的速率和效率降低。用泛酸衍生物(磷酸泛酸、泛硫乙胺、泛醇)治疗肥胖大鼠,可增强丙酮酸和脂肪酸肉碱酯的氧化磷酸化。在所研究的化合物中,泛醇更有效地激活了呼吸控制和磷酸化速率。此外,泛醇而非磷酸泛酸或泛硫乙胺,增加了肉碱棕榈酰转移酶1的活性,这证实了在该化合物的影响下,脂肪酸更倾向于用于线粒体氧化。