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体外培养的人脂肪细胞中游离脂肪酸再酯化的机制。

Mechanism of free fatty acid re-esterification in human adipocytes in vitro.

作者信息

Edens N K, Leibel R L, Hirsch J

机构信息

Rockefeller University, New York, NY 10021-6399.

出版信息

J Lipid Res. 1990 Aug;31(8):1423-31.

PMID:2280183
Abstract

Within adipose tissue, free fatty acids liberated by lipolysis may be re-esterified into newly synthesized triacylglycerol. We hypothesized that re-esterification may occur via an extracellular route, such that free fatty acids arising from lipolysis must leave the adipocyte and be taken up again before they can be re-esterified. We simultaneously measured rates of lipolysis, acylglycerol synthesis, and free fatty acid re-esterification in human adipose tissue and isolated adipocytes in vitro, utilizing a dual-isotopic technique. We manipulated incubations to increase mixing of released free fatty acids with the incubation medium. Such manipulations should decrease the probability that released free fatty acids would be taken up and re-esterified. We found that re-esterification was decreased in isolated adipocytes compared to fragments of tissue, in shaken compared to unshaken incubations, and in low adipocyte concentrations compared to high adipocyte concentrations. Rates of acylglycerol synthesis and lipolysis were unaltered by these manipulations, indicating that changes in free fatty acid re-esterification are not secondary to effects on these processes. The results are consistent with an extracellular route for free fatty acid re-esterification. Such a mechanism suggests that adipose tissue blood flow may play an important role in the regulation of free fatty acid release from adipose tissue.

摘要

在脂肪组织中,通过脂解作用释放的游离脂肪酸可能会重新酯化为新合成的三酰甘油。我们推测重新酯化可能通过细胞外途径发生,即脂解产生的游离脂肪酸必须离开脂肪细胞并再次被摄取,才能进行重新酯化。我们利用双同位素技术,同时测量了人体脂肪组织和体外分离的脂肪细胞中的脂解速率、酰基甘油合成速率和游离脂肪酸重新酯化速率。我们对孵育条件进行了调控,以增加释放的游离脂肪酸与孵育培养基的混合。这种调控应会降低释放的游离脂肪酸被摄取并重新酯化的概率。我们发现,与组织片段相比,分离的脂肪细胞中的重新酯化作用减弱;与未振荡的孵育相比,振荡孵育中的重新酯化作用减弱;与高脂肪细胞浓度相比,低脂肪细胞浓度下的重新酯化作用减弱。这些调控并未改变酰基甘油合成速率和脂解速率,表明游离脂肪酸重新酯化作用的变化并非这些过程所产生影响的继发结果。这些结果与游离脂肪酸重新酯化的细胞外途径一致。这样一种机制表明,脂肪组织血流量可能在调节脂肪组织游离脂肪酸释放中发挥重要作用。

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