Tappy L, Cayeux M C, Schneiter P, Schindler C, Temler E, Jéquier E, Chioléro R
Institute of Physiology, Faculty of Medicine, University of Lausanne, Switzerland.
Am J Physiol. 1995 Apr;268(4 Pt 1):E630-5. doi: 10.1152/ajpendo.1995.268.4.E630.
Hepatic glucose production is autoregulated during infusion of gluconeogenic precursors. In hyperglycemic patients with multiple trauma, hepatic glucose production and gluconeogenesis are increased, suggesting that autoregulation of hepatic glucose production may be defective. To better understand the mechanisms of autoregulation and its possible alterations in metabolic stress, lactate was coinfused with glucose in healthy volunteers and in hyperglycemic patients with multiple trauma or critical illness. In healthy volunteers, infusion of glucose alone nearly abolished endogenous glucose production. Lactate increased gluconeogenesis (as indicated by a decrease in net carbohydrate oxidation with no change in total [13C]carbohydrate oxidation) but did not increase endogenous glucose production. In patients with metabolic stress, endogenous glucose production was not suppressed by exogenous glucose, but lactate did not further increase hepatic glucose production. It is concluded that 1) in healthy humans, autoregulation of hepatic glucose production during infusion of lactate is still present when glycogenolysis is suppressed by exogenous glucose and 2) autoregulation of hepatic glucose production is not abolished in hyperglycemic patients with metabolic stress.
在输注糖异生前体物质期间，肝脏葡萄糖生成受到自动调节。在患有多发伤的高血糖患者中，肝脏葡萄糖生成和糖异生增加，这表明肝脏葡萄糖生成的自动调节可能存在缺陷。为了更好地理解自动调节机制及其在代谢应激中可能的改变，在健康志愿者以及患有多发伤或危重病的高血糖患者中，将乳酸与葡萄糖同时输注。在健康志愿者中，单独输注葡萄糖几乎完全抑制了内源性葡萄糖生成。乳酸增加了糖异生（表现为净碳水化合物氧化减少，而总[13C]碳水化合物氧化无变化），但并未增加内源性葡萄糖生成。在代谢应激患者中，外源性葡萄糖并未抑制内源性葡萄糖生成，而乳酸也未进一步增加肝脏葡萄糖生成。结论是：1）在健康人体中，当外源性葡萄糖抑制糖原分解时，输注乳酸期间肝脏葡萄糖生成的自动调节仍然存在；2）在患有代谢应激的高血糖患者中，肝脏葡萄糖生成的自动调节并未被消除。
