FREE-FATTY ACID METABOLISM AND OBESITY--IN VIVO, IN IN VITRO COMPARISONS

游离脂肪酸代谢与肥胖——体内、体外比较

• 批准号: 3964859
• 负责人: B V HOWARD
• 金额: --
• 依托单位: NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/3964859
• 关键词: adipocytes; biopsy; calorimetry; epidemiology; free fatty acids; glucose metabolism; hormone regulation /control mechanism; human subject; insulin; lipid metabolism; nutrition related tag; obesity; oxidation; radiotracer; tissue /cell culture

Free-fatty acid release from adipose tissue is the sole mechanism for the mobilization of fat cell triglyceride. Defective FFA release in obese subjects will result in the maintenance of large fat stores and the perpetuation of obesity. Excessive FFA release on the other hand might lead to increased lipoprotein formation or a worsening of reduced glucose disposal. We have used FFA turnover and lipid oxidation rate, assessment of body composition to measure total fat mass, and in vitro measurements of lipolytic rates in isolated fat cells, in the same subjects to investigate possible mechanisms of regulation of in vivo FFA metabolism. The data indicate that fatty acid availability or use per kg of fat actually decreases with increasing obesity. This could be due to a contribution of nonadipose tissue triglyceride to the FFA turnover and lipid oxidation. Even more likely, however, is that plasma or local tissue factors in obese individuals prevent fatty acid from becoming available in spite of increased stores. This was also suggested by the findings in vitro. These data suggested that the fat cells were more than capable of releasing large amounts of FFA in obese subjects but apparently failed to do so in vivo. These results indicate that in obese subjects much of the increased fat store may not be accessible to the rest of the body. Furthermore, in vitro measurements of fat cell lipolysis cannot be used to directly predict in vivo fatty acid metabolism. Finally, these data indicate that there is a large non-oxidative fatty acid disposal that may be important in the regulation of the plasma FFA concentration.

从脂肪组织释放游离脂肪酸是脂肪酸代谢的唯一机制。 脂肪细胞甘油三酯的动员。 肥胖患者FFA释放缺陷 受试者将导致维持大量脂肪储存， 肥胖的延续。 另一方面，过量的FFA释放可能 导致脂蛋白形成增加或葡萄糖减少恶化 处置 我们采用FFA周转率和脂质氧化率，评估 的身体组成来测量总脂肪量，以及体外测量 在同一研究对象中，分离脂肪细胞的脂解率 体内FFA代谢调节的可能机制。 数据 表明每公斤脂肪酸利用率或使用量实际上 随着肥胖的增加而减少。 这可能是由于 非脂肪组织甘油三酯对FFA周转和脂质氧化的影响。 然而，更有可能的是，肥胖患者的血浆或局部组织因子 个人阻止脂肪酸变得可用，尽管 增加的商店。 体外实验结果也表明了这一点。 这些 数据表明，脂肪细胞能够释放大量的 大量的FFA在肥胖的受试者，但显然未能做到这一点在体内。 这些结果表明，在肥胖受试者中， 身体的其余部分可能无法接触到存储器。 此外，在体外 脂肪细胞脂解的测量不能用于直接预测 体内脂肪酸代谢 最后，这些数据表明， 大量的非氧化性脂肪酸处理，这可能是重要的， 调节血浆FFA浓度。