Henry R R, Gumbiner B, Flynn T, Thorburn A W
Department of Medicine, Veterans Administration Medical Center, San Diego, CA 92161.
Diabetes. 1990 Feb;39(2):149-56. doi: 10.2337/diab.39.2.149.
Hyperglycemia in non-insulin-dependent diabetes mellitus (NIDDM) stimulates peripheral glucose uptake, which tends to compensate for impaired insulin-mediated glucose uptake. The metabolic fate of glucose and suppression of fat oxidation may differ, however, when glucose uptake is stimulated primarily by insulin or hyperglycemia. To address this issue, three hyperinsulinemic glucose-clamp studies were performed in combination with indirect calorimetry in seven nonobese subjects with NIDDM. In the first two experiments, when glucose uptake was matched at approximately 8 mg.kg-1 fat-free mass (FFM).min-1 with primarily hyperinsulinemia (1350 +/- 445 pM) or hyperglycemia (20.8 +/- 1.8 mM), identical rates of glucose oxidation (3.21 +/- 0.29 and 3.10 +/- 0.23 mg.kg-1 FFM.min-1, NS) and nonoxidative glucose metabolism (5.19 +/- 0.75 and 5.46 +/- 0.61 mg.kg-1 FFM.min-1, NS) were achieved. When glucose uptake was increased further to 11.11 +/- 0.36 mg.kg-1 FFM.min-1 with less insulin (625 +/- 70 pM) and hyperglycemia, glucose oxidation (3.85 +/- 0.26 mg.kg-1 FFM.min-1) and nonoxidative glucose metabolism (7.26 +/- 0.51 mg.kg-1 FFM.min-1) rose significantly (both P less than 0.05 from matched studies at lower rates of glucose uptake). During all glucose-clamp studies, free fatty acids were comparably suppressed by 40-46% (all P less than 0.005 vs. basal values), whereas fat oxidation was suppressed by 70-80% (all P less than 0.005 vs. basal values). A strong negative correlation was observed between rates of glucose and fat oxidation (r = -0.88, P less than 0.001) when all studies were combined.(ABSTRACT TRUNCATED AT 250 WORDS)
非胰岛素依赖型糖尿病（NIDDM）中的高血糖会刺激外周葡萄糖摄取，这往往会补偿胰岛素介导的葡萄糖摄取受损。然而，当葡萄糖摄取主要由胰岛素或高血糖刺激时，葡萄糖的代谢命运和脂肪氧化的抑制可能会有所不同。为了解决这个问题，对7名非肥胖NIDDM患者进行了三项高胰岛素-正葡萄糖钳夹研究，并结合间接测热法。在前两个实验中，当葡萄糖摄取量以约8mg·kg-1去脂体重（FFM）·min-1相匹配时，主要通过高胰岛素血症（1350±445pM）或高血糖（20.8±1.8mM）实现，葡萄糖氧化率（3.21±0.29和3.10±0.23mg·kg-1FFM·min-1，无显著性差异）和非氧化葡萄糖代谢率（5.19±0.75和5.46±0.61mg·kg-1FFM·min-1，无显著性差异）相同。当用较少的胰岛素（625±70pM）和高血糖将葡萄糖摄取量进一步提高到11.11±0.36mg·kg-1FFM·min-1时，葡萄糖氧化率（3.85±0.26mg·kg-1FFM·min-1）和非氧化葡萄糖代谢率（7.26±0.51mg·kg-1FFM·min-1）显著升高（与较低葡萄糖摄取率的匹配研究相比，两者P均小于0.05）。在所有葡萄糖钳夹研究期间，游离脂肪酸被同等程度地抑制了40 - 46%（与基础值相比，所有P均小于0.005），而脂肪氧化被抑制了70 - 80%（与基础值相比，所有P均小于0.005）。当所有研究合并时，观察到葡萄糖氧化率和脂肪氧化率之间存在很强的负相关（r = -0.88，P小于0.001）。（摘要截断于250字）
