Frayn K N, Shadid S, Hamlani R, Humphreys S M, Clark M L, Fielding B A, Boland O, Coppack S W
Nuffield Department of Clinical Medicine, Radcliffe Infirmary, Oxford, United Kingdom.
Am J Physiol. 1994 Mar;266(3 Pt 1):E308-17. doi: 10.1152/ajpendo.1994.266.3.E308.
There is net outward flow of fatty acids from adipose tissue in the fasted state but net inward flow and storage in the postprandial state. We investigated how this is regulated. Arteriovenous differences were measured across a subcutaneous adipose depot in six normal subjects before and for 5 h after a meal containing 80 g fat and 80 g carbohydrate. In five further experiments, insulin was infused at 40 mU.m-2.min-1 from 30 min after the meal, clamping the plasma glucose. Net transcapillary fatty acid flow changed from negative (outward flow from tissue to capillaries) in the postabsorptive state to consistently positive (net inward flow, implying fat storage) after the meal despite continued net efflux of fatty acids into venous blood. In the "clamped" experiments (with additional insulin), net fatty acid efflux in the venous blood was suppressed and positive transcapillary flux (storage) was more marked. Regulation of fatty acid flow appeared to depend on coordinated changes in hormone-sensitive lipase (HSL) and lipoprotein lipase (LPL) action and fatty acid esterification. Additional insulin caused no further suppression of HSL or activation of LPL but markedly stimulated fatty acid retention (presumed to represent esterification). In the absence of additional insulin, a high proportion of the fatty acids liberated by LPL are released into the venous plasma in both postabsorptive and postprandial states. We hypothesize that this "loss" of fatty acids is necessary to give precise control to the pathway of fat storage.
在禁食状态下,脂肪酸从脂肪组织有净外流,但在餐后状态下有净内流并储存。我们研究了其调节方式。在六名正常受试者进食含80克脂肪和80克碳水化合物的餐后,测量了皮下脂肪库前后的动静脉差异,并持续测量5小时。在另外五个实验中,从餐后30分钟开始以40 mU·m-2·min-1的速率输注胰岛素,以钳制血浆葡萄糖水平。尽管脂肪酸持续净流出进入静脉血,但毛细血管脂肪酸净流量从吸收后状态的负值(从组织向毛细血管的外流)变为餐后始终为正值(净内流,意味着脂肪储存)。在“钳制”实验(额外添加胰岛素)中,静脉血中脂肪酸的净流出受到抑制,毛细血管正向通量(储存)更为明显。脂肪酸流动的调节似乎取决于激素敏感性脂肪酶(HSL)和脂蛋白脂肪酶(LPL)作用以及脂肪酸酯化的协同变化。额外添加胰岛素并未进一步抑制HSL或激活LPL,但显著刺激了脂肪酸潴留(推测代表酯化)。在没有额外胰岛素的情况下,无论是在吸收后还是餐后状态,LPL释放的大部分脂肪酸都会释放到静脉血浆中。我们推测,脂肪酸的这种“损失”对于精确控制脂肪储存途径是必要的。