Insulin secretion during and after pregnancy in patients with gestational diabetes mellitus.
Insulin secretion during and after pregnancy in patients with gestational diabetes mellitus.
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DOI：
10.1210/jcem.86.2.7137
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发表时间：
2001-02
期刊：
影响因子：
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通讯作者：
C. Homko;E. Sivan;Xinhua Chen;Reece Ea;G. Boden
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文献类型：
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作者：
C. Homko;E. Sivan;Xinhua Chen;Reece Ea;G. Boden
我们测定了7名妊娠期糖尿病（GDM）患者以及8名年龄和体重匹配的非糖尿病孕妇在妊娠晚期（妊娠第三个月）和产后的肝前胰岛素分泌率（ISR）。通过静脉输注葡萄糖（高血糖钳夹）将血浆葡萄糖浓度升高至约8.9 mM，并使用在妊娠晚期和产后从每位患者获得的C肽动力学参数，通过外周C肽浓度的去卷积来测定ISR。采用一种与胰岛素原交叉反应性极小（<0.2%）的抗体，通过放射免疫分析（RIA）测量血浆胰岛素水平。在妊娠晚期，GDM患者比非糖尿病对照者胰岛素抵抗更严重，并且在高血糖反应下，ISR显著更低（689比849 pmol/min，P < 0.05），葡萄糖摄取率也更低（30.6比49.4 μmol/kg·min，P < 0.05）。产后，GDM患者和对照者的ISR和胰岛素抵抗均下降（ISR分别下降43%和43%，胰岛素抵抗分别下降75%和118%），并且两组的ISR相似（352比408 pmol/min，无显著差异）。然而，GDM患者仍然比对照者胰岛素抵抗更严重。总之，妊娠晚期的GDM患者不仅ISR严重不足，而且比对照者胰岛素抵抗更严重。产后，两组的胰岛素抵抗和ISR（以及血浆胰岛素水平）均有所改善，GDM患者和对照者的ISR（以及血浆胰岛素水平）不再有显著差异。然而，GDM患者的胰岛素抵抗仍然较高，其葡萄糖摄取仍然较低。我们得出结论，GDM患者存在主要的β细胞缺陷，这使得她们无法代偿在妊娠晚期出现的胰岛素抵抗水平的升高。
We have determined prehepatic insulin secretion rates (ISRs) in seven patients with gestational diabetes mellitus (GDM) and in eight age- and weight-matched nondiabetic pregnant women during late gestation (third trimester) and again postpartum. Plasma glucose concentrations were raised to approximately 8.9 mM with iv glucose (hyperglycemic clamping), and ISRs were determined by deconvolution of peripheral C-peptide concentrations using C-peptide kinetic parameters that were obtained in every patient during late gestation and again postpartum. Plasma insulin levels were measured by RIA with an antibody with minimal (<0.2%) cross-reactivity with proinsulin. During late gestation, women with GDM were more insulin resistant than nondiabetic controls and had significantly lower ISRs (689 vs. 849 pmol/min, P < 0.05) and glucose uptake rates (30.6 vs. 49.4 micromol/kg.min, P < 0.05) in response to hyperglycemia. Postpartum, ISRs and insulin resistance decreased in women with GDM and controls (ISR by 43% and 43%, respectively, and insulin resistance by 75% and 118%, respectively), and both groups had similar ISRs (352 vs. 408 pmol/min, nonsignificant). Women with GDM, however, continued to be more insulin resistant than controls. In summary, patients with GDM during late pregnancy not only had severe deficiencies in ISR but, in addition, were more insulin resistant than controls. Postpartum, insulin resistance and ISRs (and plasma insulin levels) improved in both groups, and ISRs (and plasma insulin levels) were no longer significantly different in patients with GDM and controls. Insulin resistance, however, remained higher in women with GDM, and their glucose uptake remained lower. We concluded that the women with GDM had a major ss-cell defect that made it impossible for them to compensate for their increased level of insulin resistance, which occurred during late pregnancy.