Leonce J, Brockton N, Robinson S, Venkatesan S, Bannister P, Raman V, Murphy K, Parker K, Pavitt D, Teoh T G, Regan L, Burchell A, Steer P, Johnston D G
Metabolic Medicine and Obstetrics, Imperial College London, St. Mary's Hospital, Praed Street, London W2 1NY, UK.
Placenta. 2006 Apr;27 Suppl A:S103-8. doi: 10.1016/j.placenta.2006.02.006.
Glucose transfer from mother to fetus by placental facilitated diffusion is the dominant mechanism by which the fetus acquires glucose. In small for gestational age pregnancies, fetal glucose concentrations tend to be lower than normal and this persists following delivery. GLUT1 is the major glucose transporter in human placenta but there is no evidence of GLUT1 deficiency as a cause of the lower fetal glucose concentration in small for gestational age pregnancy. The physiological and pathological roles of the other glucose transporters (and there are 14 currently described) are unknown. In recent years, the possibility has been raised that the placenta is itself capable of supplying glucose for fetal needs. This hypothesis derived from glucose isotope studies in normal pregnancy, where dilution of glucose isotope was demonstrated in blood samples taken from the fetal circulation during intravenous infusion of glucose isotope in the mother. Although other gluconeogenic enzymes were known to be present, the placenta was previously considered incapable of glucose secretion because it lacked functional glucose-6-phosphatase. Recent studies, however, have suggested that specific glucose-6-phosphatase may be present in placenta but it may be the product of a different gene from conventional hepatic glucose-6-phosphatase. The presence of the specific transporters necessary for glucose-6-phosphatase activity is currently being investigated. The role of placental glucose secretion in normal and growth-restricted pregnancies is an area of current study.
通过胎盘易化扩散将葡萄糖从母体转运至胎儿是胎儿获取葡萄糖的主要机制。在小于胎龄儿妊娠中，胎儿血糖浓度往往低于正常水平，且这种情况在分娩后仍会持续。葡萄糖转运蛋白1（GLUT1）是人类胎盘中主要的葡萄糖转运体，但没有证据表明GLUT1缺乏是小于胎龄儿妊娠中胎儿血糖浓度降低的原因。其他葡萄糖转运体（目前已描述的有14种）的生理和病理作用尚不清楚。近年来，有人提出胎盘本身能够为胎儿需求提供葡萄糖这一可能性。这一假说源于正常妊娠中的葡萄糖同位素研究，在给母体静脉输注葡萄糖同位素期间，从胎儿循环采集的血样中证实了葡萄糖同位素的稀释。尽管已知存在其他糖异生酶，但胎盘以前被认为无法分泌葡萄糖，因为它缺乏功能性葡萄糖-6-磷酸酶。然而，最近的研究表明，胎盘可能存在特异性葡萄糖-6-磷酸酶，但它可能是与传统肝脏葡萄糖-6-磷酸酶不同基因的产物。目前正在研究葡萄糖-6-磷酸酶活性所需的特异性转运体的存在情况。胎盘葡萄糖分泌在正常和生长受限妊娠中的作用是当前的研究领域。
