Christiansen E, Andersen H B, Rasmussen K, Christensen N J, Olgaard K, Kirkegaard P, Tronier B, Vølund A, Damsbo P, Burcharth F
Department of Internal Medicine, Herlev Hospital, University of Copenhagen, Denmark.
Am J Physiol. 1993 Mar;264(3 Pt 1):E441-9. doi: 10.1152/ajpendo.1993.264.3.E441.
beta-Cell function and glucose metabolism were studied in eight insulin-dependent diabetic recipients of combined segmental pancreas and kidney transplant with peripheral insulin delivery (Px), in eight nondiabetic kidney-transplant individuals (Kx), and in eight normal subjects (Ns) after three consecutive mixed meals. All subjects had normal fasting plasma glucose, but increased basal levels of C-peptide were demonstrated in the transplant groups (P < 0.05 relative to Ns). Postprandial hyperglycemia was increased 14% in Kx and 32% in Px (P < 0.05), whereas compared with Ns postprandial C-peptide levels were increased three- and twofold, respectively, in Kx and Px (P < 0.05). Compared with Ns basal insulin secretion rate (combined model) was increased 2-fold in Kx and 1.4-fold in Px (P < 0.05). Maximal insulin secretion rate was reduced 25% in Px compared with Kx (P < 0.05) but not different from that of Ns (P NS). Also, maximal insulin secretion rate occurred later in Px than in controls (Tmax: Px 50 min, Kx 30 min, and Ns 32 min; P < 0.05). The total integrated insulin secretion was increased 1.4-fold in Px compared with Ns (P < 0.05) but decreased 1.4-fold compared with Kx (P < 0.05). Fasting and postprandial proinsulin-to-C-peptide molar ratios were inappropriately increased in Px compared with Kx and Ns. Basal hepatic glucose production was increased 43% in Px and 33% in Kx compared with Ns (P < 0.05). Postprandial total systemic glucose appearance was similar in all three groups, whereas peripheral glucose disposal was 15% reduced in Px (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
在八名接受了节段性胰腺和肾脏联合移植并采用外周胰岛素输注(Px)的胰岛素依赖型糖尿病患者、八名非糖尿病肾移植个体(Kx)以及八名正常受试者(Ns)中,研究了连续三餐后β细胞功能和葡萄糖代谢情况。所有受试者空腹血糖均正常,但移植组基础C肽水平升高(相对于Ns,P < 0.05)。Kx餐后高血糖升高14%,Px升高32%(P < 0.05),而与Ns相比,Kx和Px餐后C肽水平分别升高了三倍和两倍(P < 0.05)。与Ns相比,Kx基础胰岛素分泌率(联合模型)升高了两倍,Px升高了1.4倍(P < 0.05)。与Kx相比,Px最大胰岛素分泌率降低了25%(P < 0.05),但与Ns无差异(P无显著性差异)。此外,Px最大胰岛素分泌率出现的时间比对照组晚(达峰时间:Px为分钟,Kx为30分钟,Ns为32分钟;P < 0.05)。与Ns相比,Px总胰岛素分泌积分增加了1.4倍(P < 0.05),但与Kx相比降低了1.4倍(P < 0.05)。与Kx和Ns相比,Px空腹和餐后胰岛素原与C肽的摩尔比升高不当。与Ns相比,Px基础肝葡萄糖生成增加了43%,Kx增加了33%(P < 0.05)。三组餐后全身葡萄糖总出现率相似,而Px外周葡萄糖处置降低了15%(P < 0.05)。(摘要截选至250字)