Santiago J V, Clarke W L, Arias F
Am J Obstet Gynecol. 1978 Oct 15;132(4):455-63. doi: 10.1016/0002-9378(78)90784-6.
To determine the potential of an artificial pancreatic beta cell simulator as a therapeutic and research tool we have used the device for short-term monitoring and control of blood glucose concentrations in five pregnant patients with juvenile-onset diabetes (White's Class C) and three pregnant patients with maturity-onset diabetes (Class B). One patient with brittle juvenile-onset diabetes had successful control before, during, and after cesarean section. The other seven patients were studied during the third trimester of pregnancy and at least four weeks before delivery. Blood glucose control with Biostator regulation was excellent (mean, 96 mg. per deciliter; range, 85 to 107). The insulin requirements needed to achieve optimal glucose control with the Biostator were highly variable (range, 20 to 157 U. per 24 hours) but very similar to those previously calculated to provide optimal control by conventional means. Insulin requirements were unrelated to plasma growth hormone, placental lactogen, or glucagon concentrations. The greatest degree of insulin resistance was seen in obese patients with endogenous insulin-secretory capacity. This study indicates that a pancreatic beta cell simulator can normalize glucose concentrations and rapidly estimate daily insulin requirements in pregnant diabetic patients. In addition, the data suggest that exogenous insulin may indirectly suppress endogenous insulin secretion and thus contribute to the "insulin resistance" of obese patients with maturity-onset diabetes.
为了确定人工胰腺β细胞模拟器作为一种治疗和研究工具的潜力,我们使用该设备对5名青少年发病型糖尿病(怀特C级)孕妇和3名成年发病型糖尿病(B级)孕妇的血糖浓度进行了短期监测和控制。1例脆性青少年发病型糖尿病患者在剖宫产术前、术中及术后血糖控制成功。对其他7名患者在妊娠晚期和分娩前至少4周进行了研究。通过生物调节器进行血糖控制效果极佳(平均每分升96毫克;范围为85至107)。使用生物调节器实现最佳血糖控制所需的胰岛素需求量变化很大(范围为每24小时20至157单位),但与之前通过传统方法计算得出的提供最佳控制所需的胰岛素量非常相似。胰岛素需求量与血浆生长激素、胎盘催乳素或胰高血糖素浓度无关。在具有内源性胰岛素分泌能力的肥胖患者中观察到最大程度的胰岛素抵抗。这项研究表明,胰腺β细胞模拟器可以使糖尿病孕妇的血糖浓度正常化,并快速估计每日胰岛素需求量。此外,数据表明外源性胰岛素可能间接抑制内源性胰岛素分泌,从而导致成年发病型糖尿病肥胖患者出现“胰岛素抵抗”。