Björkman O, Eriksson L S
J Clin Invest. 1985 Jul;76(1):87-92. doi: 10.1172/JCI111982.
A brief period of starvation (2-3) depletes the hepatic glycogen stores but results in only a limited reduction of the muscle glycogen depots. In this situation insulin resistance contributes to the glucose intolerance, but it is not known which tissue or tissues are responsible for the decreased insulin sensitivity. The present study was therefore undertaken to examine the influence of a 60-h fast on insulin sensitivity in splanchnic and peripheral tissues in normal humans. Euglycemic (95 mg/dl) 1-mU insulin and hyperglycemic (215-225 mg/dl) glucose clamp studies were conducted for 2 h in overnight (12 h) and prolonged (60 h) fasted nonobese subjects. Splanchnic exchange of glucose and gluconeogenic precursors was measured using the hepatic vein catheter technique. During the euglycemic clamp, insulin infusion resulted in similar steady state insulin levels in 60-h and 12-h fasted subjects (73 +/- 7 vs. 74 +/- 5 microU/ml). Total glucose disposal was reduced by 45% after 60 h of fasting (4.0 +/- 0.3 vs. 7.6 +/- 1.1 mg/kg per min, P less than 0.05) and the splanchnic glucose balance reverted from a net release in the basal state (12 h fast, -1.7 +/- 0.2, and 60-h fast, -0.9 +/- 0.1 mg/kg per min, P less than 0.01) to a net uptake during the clamps that was similar after 60 h and 12 h of fasting (0.6 +/- 0.1 vs. 0.6 +/- 0.2 mg/kg per min). During the hyperglycemic clamp, insulin levels rose rapidly in all subjects. In the 12-h fasted group this rise was followed by a further gradual one, reaching significantly higher values than in 60-h fasted subjects during the second hour (67 +/- 15 vs. 25 +/- 2 microU/ml, P less than 0.05). Total glucose disposal was lower, though not significantly so, after the 60-h fast (2.6 +/- 0.4 vs. 5.4 +/- 1.3 mg/kg per min, 0.05 less than P less than 0.10), and as with the euglycemic clamp, the splanchnic glucose balance was altered from a basal net release to a net uptake during the clamp (1.3 +/- 0.2 vs. 1.1 +/- 0.2 mg/kg per min). After an overnight fast, splanchnic lactate uptake fell and the arterial lactate concentration rose in response to both hyperglycemia and hyperinsulinemia, whereas these variables were unchanged in the 60-h fasted subjects during both types of clamp studies.
短期饥饿（2 - 3天）会耗尽肝脏糖原储备，但只会使肌肉糖原储备有有限程度的减少。在这种情况下，胰岛素抵抗会导致葡萄糖不耐受，但尚不清楚是哪个或哪些组织导致胰岛素敏感性降低。因此，本研究旨在探讨60小时禁食对正常人体内内脏和外周组织胰岛素敏感性的影响。对过夜（12小时）和长期（60小时）禁食的非肥胖受试者进行了2小时的正常血糖（95毫克/分升）1微单位胰岛素和高血糖（215 - 225毫克/分升）葡萄糖钳夹研究。使用肝静脉导管技术测量内脏葡萄糖和糖异生前体的交换。在正常血糖钳夹期间，胰岛素输注使60小时和12小时禁食受试者的稳态胰岛素水平相似（73±7对74±5微单位/毫升）。禁食60小时后，总葡萄糖处置量降低了45%（4.0±0.3对7.6±1.1毫克/千克每分钟，P<0.05），内脏葡萄糖平衡从基础状态（12小时禁食，-1.7±0.2，60小时禁食，-0.9±0.1毫克/千克每分钟，P<0.01）的净释放转变为钳夹期间的净摄取，60小时和12小时禁食后的净摄取相似（0.6±0.1对0.6±0.2毫克/千克每分钟）。在高血糖钳夹期间，所有受试者的胰岛素水平迅速上升。在12小时禁食组中，这种上升之后还有进一步的逐渐上升，在第二小时达到显著高于60小时禁食受试者的值（67±15对25±2微单位/毫升，P<0.05）。禁食60小时后，总葡萄糖处置量较低，尽管差异不显著（2.6±0.4对5.4±1.3毫克/千克每分钟，0.05<P<0.10），并且与正常血糖钳夹一样，内脏葡萄糖平衡从基础净释放转变为钳夹期间的净摄取（1.3±0.2对1.1±0.2毫克/千克每分钟）。过夜禁食后，内脏乳酸摄取减少，动脉乳酸浓度在高血糖和高胰岛素血症时均升高，而在两种钳夹研究期间，这些变量在60小时禁食受试者中保持不变。
