Carver T D, Quick A A, Teng C C, Pike A W, Fennessey P V, Hay W W
Division of Perinatal Medicine, University of Colorado Health Sciences Center, Denver 80262, USA.
Am J Physiol. 1997 Jan;272(1 Pt 1):E107-17. doi: 10.1152/ajpendo.1997.272.1.E107.
We measured leucine flux rates during infusions of L-[1-14C]- and L-[1-1C]leucine in fetal sheep exposed to maternal insulin-induced hypoglycemia over the last 8 wk (40%) of gestation to determine effects of chronic glucose deficiency and hypoglycemia on fetal leucine metabolism. Compared with control fetuses (C, n = 5), hypoglycemic fetuses (HG, n = 8) weighed less (C, 3.43 +/- 0.07 kg; HG, 2.32 +/- 0.24 kg), had lower plasma glucose (C, 1.04 +/- 0.02 mM; HG, 0.59 +/- 0.01 mM), insulin (C, 48 +/- 6 pM; HG, 12 +/- 6 pM), and leucine concentrations (C, 195.6 +/- 8.3 microM; HG, 140.8 +/- 15.0 microM), lower rates of net leucine uptake (C, 4.2 +/- 0.6 mumol.min-1.kg-1; HG, 2.1 +/- 0.4 mumol.min-1.kg-1) and leucine flux into protein accretion (C, 2.8 +/- 0.2 mumol.min-1.kg-1; HG, 0.6 +/- 0.1 mumol.min-1.kg-1), and an increased rate of leucine release from protein breakdown (C, 1.1 +/- 0.1 mumol.min-1.kg-1; HG, 3.3 +/- 0.2 mumol.min-1.kg-1) (P < 0.05 for all). Plasma leucine disposal, flux into protein synthesis, and oxidation were not different between groups. We conclude that adaptations of fetal leucine metabolism to long-term hypoglycemia and decreased glucose apply represent diminished leucine uptake and increased leucine release from protein breakdown, which are associated with decreased incorporation of leucine into protein accretion and a slower rate of fetal growth.
我们在妊娠最后8周（40%）暴露于母体胰岛素诱导低血糖的胎羊中，输注L-[1-¹⁴C]-和L-[1-¹³C]亮氨酸期间测量亮氨酸通量率，以确定慢性葡萄糖缺乏和低血糖对胎儿亮氨酸代谢的影响。与对照胎儿（C组，n = 5）相比，低血糖胎儿（HG组，n = 8）体重较轻（C组，3.43±0.07 kg；HG组，2.32±0.24 kg），血糖（C组，1.04±0.02 mM；HG组，0.59±0.01 mM）、胰岛素（C组，48±6 pM；HG组，12±6 pM）和亮氨酸浓度较低（C组，195.6±8.3 μM；HG组，140.8±15.0 μM），亮氨酸净摄取率（C组，4.2±0.6 μmol·min⁻¹·kg⁻¹；HG组，2.1±0.4 μmol·min⁻¹·kg⁻¹）和亮氨酸流入蛋白质合成的通量较低（C组，2.8±0.2 μmol·min⁻¹·kg⁻¹；HG组，0.6±0.1 μmol·min⁻¹·kg⁻¹），蛋白质分解产生的亮氨酸释放率增加（C组，1.1±0.1 μmol·min⁻¹·kg⁻¹；HG组，3.3±0.2 μmol·min⁻¹·kg⁻¹）（所有P<0.05）。两组之间血浆亮氨酸处置率、流入蛋白质合成的通量和氧化率无差异。我们得出结论，胎儿亮氨酸代谢对长期低血糖和葡萄糖供应减少的适应性表现为亮氨酸摄取减少和蛋白质分解产生的亮氨酸释放增加，这与亮氨酸掺入蛋白质合成减少和胎儿生长速度减慢有关。
