FREE-FATTY ACID METABOLISM AND OBESITY

FFA周转率测量与脂质氧化率结合 和身体成分的评估被用来调查 体内FFA代谢调节的可能机制， FFA代谢之间的相互关系， 碳水化合物和脂蛋白。 我们之前的研究表明 肥胖者每克脂肪的游离脂肪酸动员量较少。 我们还发现，脂肪酸的一个重要组成部分 周转是非氧化性处置。 进一步审查 控制游离脂肪酸的机制，我们进行了 两种代谢条件下游离脂肪酸周转的研究 扰动 一种是普萘洛尔的注射， 是比较高饱和脂肪和低脂肪的个体， 高碳水化合物饮食。 普萘洛尔输注降低了 营业额的游离脂肪酸，这种影响是更大的， 肥胖的人 在普萘洛尔输注期间， 也增加了，因此大大减少了 非氧化性脂肪酸处理的比例。 在转移期间 高饱和脂肪的饮食，脂肪酸的生产率也 下降，脂质氧化增加，从而导致 非氧化性脂肪酸处理的比例显著降低。 数据表明交感神经系统在 调节脂肪储存中脂肪酸的输出， 肥胖的个体可能对这个问题的敏感性不同， 调控 最后，脂肪酸的非氧化成分 代谢较低的情况下，脂质氧化是 增加 这可能反映了甘油三酯再合成的抑制作用。 脂肪组织以外部位的酯化作用。

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.