Bratusch-Marrain P R, DeFronzo R A
Horm Metab Res. 1986 Mar;18(3):185-9. doi: 10.1055/s-2007-1012266.
The effect of physiologic elevations of plasma hydroxybutyrate induced by the infusion of sodium D,L-beta-hydroxybutyrate (15 mumol X kg-1 X min-1) on carbohydrate metabolism was examined with the euglycemic insulin clamp technique in nine healthy volunteers. Plasma insulin concentration was acutely raised and maintained at 126 +/- 6 microU/ml and plasma glucose was held constant at the fasting level by a variable glucose infusion. Glucose uptake of 6.53 +/- 0.80 mg X kg-1 X min-1 was unchanged by hyperketonemia when compared with an intraindividual control study using saline instead of beta-OH-butyrate infusion (6.26 +/- 0.59 mg X kg-1 X min-1). In studies, in which the degree of metabolic alkalosis accompanying butyrate infusion was mimicked by the continuous administration of bicarbonate, glucose uptake was also unaffected (6.25 +/- 0.45 mg X kg-1 X min-1). Furthermore, hyperketonemia had no effect on basal glucose production or the suppression of hepatic glucose production following hyperinsulinemia. It is concluded that moderate elevations in plasma beta-hydroxy-butyrate do not alter hepatic or peripheral glucose metabolism.
采用正常血糖胰岛素钳夹技术,在9名健康志愿者中研究了静脉输注D,L-β-羟基丁酸钠(15μmol·kg⁻¹·min⁻¹)诱导的血浆β-羟基丁酸生理性升高对碳水化合物代谢的影响。通过可变葡萄糖输注使血浆胰岛素浓度急性升高并维持在126±6μU/ml,同时使血浆葡萄糖保持在空腹水平。与使用生理盐水而非β-羟基丁酸盐输注的个体内对照研究(6.26±0.59mg·kg⁻¹·min⁻¹)相比,高酮血症时葡萄糖摄取量为6.53±0.80mg·kg⁻¹·min⁻¹,未发生改变。在通过持续输注碳酸氢盐模拟伴随丁酸盐输注的代谢性碱中毒程度的研究中,葡萄糖摄取也未受影响(6.25±0.45mg·kg⁻¹·min⁻¹)。此外,高酮血症对基础葡萄糖生成或高胰岛素血症后肝葡萄糖生成的抑制均无影响。结论是,血浆β-羟基丁酸的适度升高不会改变肝脏或外周葡萄糖代谢。