Catalano P M, Drago N M, Amini S B
Department of Reproductive Biology, Case Western Reserve University, MetroHealth Medical Center, Cleveland, OH 44109, USA.
Diabetes Care. 1998 Mar;21(3):403-8. doi: 10.2337/diacare.21.3.403.
To evaluate basal pancreatic beta-cell secretion and suppression during infused insulin and the metabolic clearance rate of insulin in women with normal and abnormal glucose tolerance prior to conception and during pregnancy.
Seven women with normal glucose tolerance and nine women with abnormal glucose tolerance during gestation were evaluated prior to conception, in early (12-14 weeks) and late (34-36 weeks) gestation. Basal insulin and C-peptide were measured after an 11-h fast and during the last 40 min of a 2-h hyperinsulinemic-euglycemic clamp at 40 mU.m-2.m-1. Suppression of basal C-peptide was calculated as the steady-state C-peptide/basal C-peptide. The metabolic clearance rate of insulin was calculated by dividing the insulin infusion rate by the steady-state insulin concentration, which was corrected for residual beta-cell secretion.
No significant differences were noted in the following parameters between women with normal and abnormal glucose tolerance with advancing gestation: increase in basal insulin (P = 0.20) and C-peptide (P = 0.12), ability of infused insulin to decrease basal C-peptide concentration (P = 0.22), and metabolic clearance rate of insulin (P = 0.76). There was a significant 65% increase in both basal insulin (P = 0.0005) and C-peptide (P = 0.0002) concentrations in all subjects with advancing gestation. There was a significant (P = 0.0001) decrease in the ability of the infused insulin to decrease basal C-peptide concentration. C-peptide as a percentage of the basal was 64% before conception, 74% in early pregnancy, and 108% in late pregnancy. The metabolic clearance rate of insulin significantly (P = 0.0005) increased with advancing gestation: pregravid 442 ml.m-2.min-1, early pregnancy 514 ml.m-2. min-1, and 526 ml.m-2.min-1 in late pregnancy.
Pregnancy is accompanied by progressive alterations in insulin kinetics, which are partly responsible for the hyperinsulinemia of this condition. These alterations are more likely a homeostatic response to the increased physiological insulin resistance of pregnancy.
评估孕前及孕期糖耐量正常和异常的女性基础胰腺β细胞分泌、胰岛素输注期间的抑制情况以及胰岛素的代谢清除率。
对7名糖耐量正常的女性和9名孕期糖耐量异常的女性在孕前、孕早期（12 - 14周）和孕晚期（34 - 36周）进行评估。在禁食11小时后以及在40 mU·m⁻²·m⁻¹的2小时高胰岛素 - 正常血糖钳夹的最后40分钟测量基础胰岛素和C肽。基础C肽的抑制率计算为稳态C肽/基础C肽。胰岛素的代谢清除率通过将胰岛素输注速率除以稳态胰岛素浓度来计算，该浓度已针对残余β细胞分泌进行校正。
随着孕周增加，糖耐量正常和异常的女性在以下参数方面无显著差异：基础胰岛素增加量（P = 0.20）和C肽增加量（P = 0.12）、输注胰岛素降低基础C肽浓度的能力（P = 0.22）以及胰岛素的代谢清除率（P = 0.76）。所有受试者随着孕周增加，基础胰岛素（P = 0.0005）和C肽（P = 0.0002）浓度均显著增加65%。输注胰岛素降低基础C肽浓度的能力显著下降（P = 0.0001）。C肽占基础值的百分比在孕前为64%，孕早期为74%，孕晚期为108%。胰岛素的代谢清除率随着孕周增加显著增加（P = 0.0005）：孕前为442 ml·m⁻²·min⁻¹，孕早期为514 ml·m⁻²·min⁻¹，孕晚期为526 ml·m⁻²·min⁻¹。
妊娠伴随着胰岛素动力学的逐渐改变，这在一定程度上导致了该状态下的高胰岛素血症。这些改变更可能是对妊娠期间生理胰岛素抵抗增加的一种稳态反应。
