Hagström-Toft E, Arner P, Näslund B, Ungerstedt U, Bolinder J
Department of Medicine, Huddinge Hospital, Sweden.
Diabetes. 1991 Jun;40(6):666-72. doi: 10.2337/diab.40.6.666.
The effects of insulin deprivation and replacement on adipose tissue metabolism were investigated in vivo with microdialysis in nine insulin-dependent diabetic patients with no residual insulin secretion. Dialysis probes, implanted in abdominal subcutaneous fat, were continuously perfused, and tissue dialysate concentrations of glycerol (lipolysis index), glucose, lactate, and pyruvate were determined. Comparisons were made with respective metabolite levels in venous plasma. After termination of intravenous insulin infusion, free insulin in plasma fell from 130 to 70 pM. At the same time, glucose levels in plasma and adipose tissue rose in parallel. However, the relative increase in glucose levels was greater in adipose tissue than in blood. On the other hand, the increase in glycerol concentration in adipose tissue (35%) was markedly less than that in venous plasma (250%). Lactate and pyruvate levels in adipose tissue and blood remained unchanged. After the resumption of intravenous insulin, free insulin in plasma rose to approximately 600 pM. At the same time, the glucose levels in blood and adipose tissue decreased rapidly, and the glycerol concentration in these tissues decreased to 50% of the baseline levels. The lactate and pyruvate levels in subcutaneous tissue increased briefly after insulin replacement, whereas the lactate but not pyruvate levels in blood showed a similar increase. The alpha- or beta-blocking agents phentolamine and propranolol in the ingoing tissue perfusate did not influence tissue glycerol at any time during the experiment. We concluded that insulin-induced changes in circulating metabolites only partly reflect variations in adipose tissue substrate kinetics. During insulin deprivation, glucose is accumulated in the adipose tissue extracellular compartment, probably because of reduced utilization by the adipocytes.(ABSTRACT TRUNCATED AT 250 WORDS)
在9例无残余胰岛素分泌的胰岛素依赖型糖尿病患者体内,采用微透析技术研究了胰岛素缺乏及补充对脂肪组织代谢的影响。将透析探针植入腹部皮下脂肪,持续灌注,测定组织透析液中甘油(脂解指数)、葡萄糖、乳酸和丙酮酸的浓度,并与静脉血浆中相应代谢物水平进行比较。静脉输注胰岛素终止后,血浆中游离胰岛素从130 pM降至70 pM。与此同时,血浆和脂肪组织中的葡萄糖水平平行升高。然而,脂肪组织中葡萄糖水平的相对升高幅度大于血液中的升高幅度。另一方面,脂肪组织中甘油浓度的升高(35%)明显低于静脉血浆中的升高(250%)。脂肪组织和血液中的乳酸和丙酮酸水平保持不变。重新静脉输注胰岛素后,血浆中游离胰岛素升至约600 pM。与此同时,血液和脂肪组织中的葡萄糖水平迅速下降,这些组织中的甘油浓度降至基线水平的50%。胰岛素补充后,皮下组织中的乳酸和丙酮酸水平短暂升高,而血液中的乳酸水平有类似升高,但丙酮酸水平未升高。在实验过程中,进入组织灌流液中的α或β阻滞剂酚妥拉明和普萘洛尔在任何时候都不影响组织甘油水平。我们得出结论,胰岛素引起的循环代谢物变化仅部分反映脂肪组织底物动力学的变化。在胰岛素缺乏期间,葡萄糖在脂肪组织细胞外间隙中积累,可能是因为脂肪细胞的利用率降低。(摘要截短至250字)