Effect of elevated free fatty acids on glucose oxidation in normal humans.
Effect of elevated free fatty acids on glucose oxidation in normal humans.
复制标题
游离脂肪酸升高对正常人葡萄糖氧化的影响。
DOI：
10.1016/0026-0495(88)90131-x
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Wolfe,RR
中科院分区：
文献类型：
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作者：
Wolfe,BM;Klein,S;Peters,EJ;Schmidt,BF;Wolfe,RR
体外研究表明，游离脂肪酸(FFA)的可获得性和葡萄糖氧化之间存在着相反的关系，这导致了葡萄糖-脂肪酸循环的提出。关于游离脂肪酸对葡萄糖氧化的影响，体内研究得出了相互矛盾的结果。在本研究中，我们测定了六名正常志愿者的游离脂肪酸对葡萄糖氧化的影响。葡萄糖摄取率通过使用恒定的葡萄糖输注来抑制内源性葡萄糖的产生来固定。在四个小时的研究中，以8毫克/公斤×分钟的速度连续注入葡萄糖，以确保几乎所有组织都将葡萄糖用作能量底物。在基线葡萄糖输注2小时后，在恒定葡萄糖输注的基础上加入20%脂肪乳剂，输注速度为1.0毫升/分钟加肝素，持续2小时。总碳水化合物的氧化用间接量热法测定，输注(血浆)葡萄糖的直接氧化用U-13C-葡萄糖测定。糖原氧化为总碳水化合物氧化与血糖氧化的差值。根据输液速度计算葡萄糖摄取量，并根据血浆和/或尿糖浓度的变化进行校正。葡萄糖摄取率接近静脉输注葡萄糖的速率，而脂肪输注的葡萄糖摄取率没有变化。游离脂肪酸对U-13C-葡萄糖氧化产生二氧化碳的百分率(74.5±12.3)%和葡萄糖摄取百分率(37.5±4.0)无明显影响。间接量热法显示脂肪摄入后1小时总碳水化合物氧化量由4.22±1.12 mg/kg×min降至3.13±1.65 mg/kg×min(P<；0.05)。糖原氧化(从未进入血浆池的葡萄糖的氧化)的计算值随着FFA利用率的增加而显著降低(0.97±1.18至0.05±1.54 mg/kg×min)(P<；0.05)。这些数据表明，当葡萄糖摄取速率恒定时，游离脂肪酸并不抑制血糖氧化。然而，循环中游离脂肪酸的增加可能通过抑制糖原的氧化来影响总葡萄糖的氧化。
In vitro studies indicating an inverse relationship between free fatty acid (FFA) availability and glucose oxidation led to proposal of the glucose-fatty acid cycle. In vivo studies have yielded conflicting results regarding the effect of FFA on glucose oxidation. In the present study the effect of FFA on glucose oxidation was determined in six normal volunteer subjects. The rate of glucose uptake was fixed by using a constant glucose infusion to suppress endogenous glucose production. Glucose was infused continuously overnight and during the four hour study at 8 mg/kg × min to ensure use of glucose as an energy substrate by virtually all tissues. Following a two-hour baseline glucose infusion, infusion of 20% IV fat emulsion at 1.0 mL/min plus heparin was added to the constant glucose infusion for two additonal hours. Total carbohydrate oxidation was determined by indirect calorimetry, and the direct oxidation of the infused (plasma) glucose was measured by the use of U-13C-glucose. Glycogen oxidation was calculated as the difference between total carbohydrate oxidation and the oxidation of plasma glucose. Glucose uptake was calculated from the infusion rate, corrected for any changes in plasma and/or urine glucose concentration. Glucose uptake closely approximated the rate of IV glucose infusion and was unchanged by fat infusion. The percent of CO2production from U-13C-glucose oxidation (74.5 ± 12.3, mean ± SD) was not affected by FFA, nor was the percent of glucose uptake oxidized (37.5 ± 4.0). Indirect calorimetry showed a decrease of total carbohydrate oxidation from 4.22 ± 1.12 mg/kg × min to 3.13 ± 1.65 mg/kg × min (P< .05) during the final hour of fat infusion. The calculated value for glycogen oxidation (the oxidation of glucose which never entered the plasma pool) significantly decreased with increased FFA availability (0.97 ± 1.18 to 0.05 ± 1.54 mg/kg × min) (P< .05). These data suggest that FFAs do not inhibit plasma glucose oxidation when the rate of glucose uptake is constant. Increases in circulating FFAs may affect total glucose oxidation, however, by suppressing the oxidation of glycogen.