Phillips D I, Borthwick A C, Stein C, Taylor R
Metabolic Programming Group, Southampton General Hospital, UK.
Diabet Med. 1996 Apr;13(4):325-9. doi: 10.1002/(SICI)1096-9136(199604)13:4<325::AID-DIA79>3.0.CO;2-S.
Growth retardation during fetal life is associated with insulin insensitivity and an increased prevalence of impaired glucose tolerance in adult life. Because insulin-mediated stimulation of glycogen synthase may be an important rate-limiting step for insulin action at the cellular level, we have sought to determine whether impaired activation of muscle glycogen synthase is linked with early growth retardation. Postprandial glycogen synthase activity was therefore measured in muscle biopsies from a group of 27 women with normal glucose tolerance aged around 50 who were born in Preston, Lancashire, whose birthweight and body size at birth were recorded. Glycogen synthase activity measured at 0.1 mmol 1(-1) glucose-6-phosphate correlated with insulin sensitivity as measured by a short insulin tolerance test (r = 0.42, p < 0.05) and the waist to hip ratio (r = -0.48, p < 0.01), but not body mass index, body fat percentage or age. Within the group of women with normal glucose tolerance there was no relationship between intra-uterine growth as evidenced by birthweight or body size at birth and the response to insulin of skeletal muscle glycogen synthase in adult life. Thus we found no evidence for a direct link between fetal growth and insulin sensitivity in this pathway.
胎儿期生长迟缓与胰岛素不敏感以及成年期糖耐量受损患病率增加有关。由于胰岛素介导的糖原合酶刺激可能是细胞水平胰岛素作用的一个重要限速步骤，我们试图确定肌肉糖原合酶激活受损是否与早期生长迟缓有关。因此，我们测量了一组27名糖耐量正常、年龄约50岁、出生于兰开夏郡普雷斯顿的女性肌肉活检样本中的餐后糖原合酶活性，并记录了她们的出生体重和出生时的身体大小。在0.1 mmol 1(-1)葡萄糖-6-磷酸浓度下测得的糖原合酶活性与通过短胰岛素耐量试验测量的胰岛素敏感性相关（r = 0.42，p < 0.05），与腰臀比相关（r = -0.48，p < 0.01），但与体重指数、体脂百分比或年龄无关。在糖耐量正常的女性群体中，出生体重或出生时身体大小所证明的子宫内生长与成年期骨骼肌糖原合酶对胰岛素的反应之间没有关系。因此，我们没有发现该途径中胎儿生长与胰岛素敏感性之间存在直接联系的证据。
