FREE-FATTY ACID METABOLISM AND OBESITY

结合脂肪氧化率的FFA周转率测定 和身体成分的评估来调查 体内游离脂肪酸代谢调控的可能机制 游离脂肪酸代谢的相互关系， 碳水化合物和脂蛋白。我们之前的研究表明 肥胖者每克脂肪的FFA动员较少。 我们还表明，脂肪酸的一个重要成分 周转率为非氧化性处置。为了进一步研究 控制游离脂肪酸的机制，我们进行了 两种代谢方式下游离脂肪酸周转率的研究 微扰。一种是普萘洛尔，另一种是心得安 是比较高饱和脂肪和低脂肪的个体， 高碳水化合物饮食。普萘洛尔输注可降低 游离脂肪酸的周转率，这种影响在越多的人中越大 肥胖的人。在心得安输注过程中，脂质氧化 也增加了，因此导致大大减少了 非氧化性脂肪酸处置比例。在转接期间 到高饱和脂肪饮食，脂肪酸的产生率也 下降，脂质氧化增加，从而导致 非氧化性脂肪酸处置比例明显降低。 数据表明交感神经系统起着一定的作用 在调节脂肪储存和脂肪的脂肪酸输出方面 肥胖者对此的敏感度可能有所不同 监管。最后，脂肪酸的非氧化成分 在脂质氧化的情况下，新陈代谢较低 增加了。这可能反映了对甘油三酯再摄取的抑制 脂肪组织以外的部位的酯化作用。

FFA turnover measurements combined with lipid oxidation rate and assessment of body composition were used to investigate possible mechanisms of regulation of in vivo FFA metabolism and the inter-relationships between the metabolisms of FFA, carbohydrate, and lipoproteins. Our previous studies had shown that FFA mobilization was less per gram of fat in obese subjects. We also showed that a significant component of fatty acid turnover was non-oxidative disposal. To further examine the mechanisms of control of free-fatty acids, we have conducted studies of free-fatty acid turnover under two metabolic perturbations. One was the infusion of propranolol and the other was comparing individuals on a high-saturated fat and a low-fat, high carbohydrate diet. Propranolol infusion decreased the turnover of free-fatty acid, and this effect was greater in more obese individuals. During propranolol infusion, lipid oxidation was also increased, resulting therefore in a greatly decreased proportion of non-oxidative fatty acid disposal. During transfer to a high saturated fat diet, fatty acid production rates also declined and lipid oxidation increased, thus resulting in a significantly lower proportion of non-oxidative fatty acid disposal. The data suggest that the sympathetic nervous system plays a role in regulating the output of fatty acids from adipose stores and that obese individuals may differ in their sensitivity to this regulation. Finally, the non-oxidative component of fatty acid metabolism was lower in situations where lipid oxidation was increased. This may reflect inhibition of triglyceride re- esterification in sites other than adipose tissue.