Differential effects of safflower oil versus fish oil feeding on insulin-stimulated glycogen synthesis, glycolysis, and pyruvate dehydrogenase flux in skeletal muscle -: A 13C nuclear magnetic resonance study
Differential effects of safflower oil versus fish oil feeding on insulin-stimulated glycogen synthesis, glycolysis, and pyruvate dehydrogenase flux in skeletal muscle -: A 13C nuclear magnetic resonance study
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DOI：
10.2337/diabetes.48.1.134
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发表时间：
1999-01-01
期刊：
影响因子：
7.7
通讯作者：
Shulman, GI
中科院分区：
文献类型：
--
作者：
Jucker, BM;Cline, GW;Shulman, GI
为了检查红花油与鱼油喂养对体内肌内葡萄糖代谢和相对丙酮酸脱氢酶（PDH）与三羧酸（TCA）循环通量的影响，对大鼠配对喂养由1）59%红花油，2）59%鲱鱼鱼油或3）59%碳水化合物（对照）组成的饮食（卡路里）。在正常血糖（类似于6 mmol/l）高胰岛素血症（类似于180 mu U/ml）钳夹期间，通过13 C核磁共振（NMR）光谱监测清醒大鼠后肢中[1-C-13]葡萄糖标记物掺入[1-C-13]糖原、[3-C-13]乳酸盐和[3-C-13]丙氨酸，评估糖酵解和糖原合成速率。乳酸盐、丙氨酸和谷氨酸盐的稳态同位素分析，用于确定在这些条件下肌肉中存在的相对PDH与TCA循环通量。与对照组和鱼油组大鼠相比，饲喂红花油组大鼠具有胰岛素抵抗，这反映在钳夹期间葡萄糖输注速率（G（inf））显著降低（21.4 +/- 2.3 vs. 31.6 +/- 2.8和31.7 +/- 1.9 mg . kg（-1）。min（-1），红花油组分别与对照组和鱼油组比较，P < 0.006）。红花油组中胰岛素刺激的葡萄糖处置的减少与较低的糖基化率（21.7 +/- 2.2 nmol . g（-1）。min（-1））与对照组（62.1 +/- 10.3 nmol . g（-1）。min（-1），P < 0.001）和鱼油（45.7 +/- 6.7 nmol . g（-1）。min（-1），P < 0.04），因为糖原合成没有变化（103 +/- 15，133 +/- 19和125 +/- 14 nmol . g（-1）。在红花油、鱼油和对照中分别检测到min（-1）。与对照组（5.2 ± 0.8 μ mol/g，P < 0.05）和鱼油组（3.6 ± 1.1 μ mol/g，P <0.01）相比，红花油组肌内甘油三酯（TG）含量增加（7.3 ± 0.8 μ mol/g）。相反地，红花油组（43 +/- 8%）与对照组（73 +/-8%，P < 0.01）和鱼油组（64 +/-6%，P < 0.05）相比，PDH对TCA循环通量的百分比降低。这些数据表明，减少胰岛素刺激的葡萄糖处置归因于红花油喂养是一个结果，减少糖酵解通量与增加相对游离脂肪酸-酮氧化与TCA循环通量，而鱼油喂养没有改变葡萄糖代谢，并可能部分是保护胰岛素刺激的葡萄糖处置限制肌内TG沉积。
To examine the effects of safflower oil versus fish oil feeding on in vivo intramuscular glucose metabolism and relative pyruvate dehydrogenase (PDH) versus tri-carboxlic acid (TCA) cycle flux, rats were pair-fed on diets consisting of 1) 59% safflower oil, 2) 59% men-haden fish oil, or 3) 59% carbohydrate (control) in calories. Rates of glycolysis and glycogen synthesis were assessed by monitoring [1-C-13]glucose label incorporation into [1-C-13]glycogen, [3-C-13]lactate, and [3-C-13]alanine in the hindlimb of awake rats via 13C nuclear magnetic resonance (NMR) spectroscopy during a euglycemic (similar to 6 mmol/l) hyperinsulinemic (similar to 180 mu U/ml) clamp. A steady-state isotopic analysis of lactate, alanine, and glutamate used to determine the relative PDH versus TCA cycle flux present in muscle under these conditions. The safflower oil-fed rats were insulin resistant compared with control and fish oil-fed rats, as reflected compared with control anf fish oil-fed rats, as reflected by a markedly reduced glucose infusion rate (G(inf)) during the clamp (21.4 +/- 2.3 vs. 31.6 +/- 2.8 and 31.7 +/- 1.9 mg . kg(-1) . min(-1) in safflower oil versus control and fish oil groups, respectively, P < 0.006). This decrease in insulin-stimulated glucose disposal in the safflower oil group was associated with a lower rate of glycosis (21.7 +/- 2.2 nmol . g(-1) . min(-1)) versus control (62.1 +/- 10.3 nmol . g(-1) . min(-1), P < 0.001) and versus fish oil (45.7 +/- 6.7 nmol . g(-1) . min(-1), P < 0.04), as no change in glycogen synthesis (103 +/- 15, 133 +/- 19, and 125 +/- 14 nmol . g(-1) . min(-1) in safflower oil, fish oil, and control, respectively) was detected. The intramuscular triglyceride (TG) content was increased in the safflower oil group (7.3 +/- 0.8 mu mol/g) compared with the control group (5.2 +/- 0.8 mu mol/g, P < 0.05) and the fish oil group (3.6 +/- 1.1 mu mol/g, P < 0.01). Conversely, the percent PDH versus TCA cycle flux was decreased in the safflower oil (43 +/- 8%) versus the control (73 +/- 8%, P < 0.01) and fish oil (64 +/- 6%, P < 0.05) groups. These data suggest that the reduced insulin-stimulated glucose disposal attributed to safflower oil feeding was a consequence of reduced glycolytic flux associated with an increase in relative free fatty acid-ketone oxidation versus TCA cycle flux, whereas fish oil feeding did not alter glucose metabolism and may in part be protective of insulin-stimulated glucose disposal by limiting intramuscular TG deposition.