Maternal semistarvation and streptozotocin-diabetes in rats have different effects on the in vivo glucose uptake by peripheral tissues in their female adult offspring
Maternal semistarvation and streptozotocin-diabetes in rats have different effects on the in vivo glucose uptake by peripheral tissues in their female adult offspring
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DOI：
10.1093/jn/127.7.1371
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发表时间：
1997-07-01
影响因子：
4.2
通讯作者：
VanAssche, FA
中科院分区：
文献类型：
--
作者：
Holemans, K;VanBree, R;VanAssche, FA
以前在人类和大鼠中的研究揭示了围产期生长迟缓和成年期葡萄糖耐受不良之间的联系。母亲半饥饿和严重的糖尿病都伴随着围产期生长迟缓的大鼠。在这项研究中，我们比较了这些条件对雌性后代组织葡萄糖摄取的影响。在吸收后状态和正常血糖高胰岛素血症期间，使用2-脱氧-[1-H-3]葡萄糖测量葡萄糖摄取，作为葡萄糖代谢指数（GMI）。在正常母鼠的成年后代的胰岛素敏感组织（5个骨骼肌、膈肌和白色脂肪组织）和两个非胰岛素敏感组织（十二指肠和脑）中测量GMI，在妊娠第11天用链脲佐菌素使母鼠患糖尿病，从妊娠第11天开始母鼠饲喂一半正常口粮。全身胰岛素抵抗，在高胰岛素血症期间降低葡萄糖输注率测量，在半饥饿大鼠（O-SR）的后代比糖尿病大鼠（O-DR）的后代轻。除胫骨前肌外，三组间任何组织的基础GMI均无差异;在高胰岛素血症期间，所有三组胰岛素敏感组织的GMI均显著升高。高胰岛素血症时骨骼肌和脂肪组织的GMI在对照组和O-SR组之间没有差异;相反，高胰岛素血症时O-DR组骨骼肌的GMI比对照组或O-SR组低25-50%。因此，母体半饥饿和糖尿病对成年雌性后代外周胰岛素敏感性有不同的影响。由于这两种情况都与围产期生长迟缓和胎儿低胰岛素血症有关，必须确定其他机制来解释糖尿病大鼠后代骨骼肌葡萄糖摄取受损。
Previous work in humans and rats has revealed a link between perinatal growth retardation and glucose intolerance in adulthood. Both maternal semistarvation and severe diabetes are accompanied by perinatal growth retardation in rats. In this study, we compared the effect of these conditions on tissue glucose uptake in their female offspring. Glucose uptake was measured as glucose metabolic index (GMI), using 2-deoxy-[1-H-3]glucose, in the postabsorptive state and during euglycemic hyperinsulinemia. The GMI was measured in insulin-sensitive tissues (5 skeletal muscles, diaphragm and white adipose tissue) and in two noninsulin-sensitive tissues (duodenum and brain) of adult offspring of normal dams, dams rendered diabetic with streptozotocin on d 11 of pregnancy, and dams fed half normal rations from d 11 of pregnancy. Whole-body insulin resistance, measured by decreased glucose infusion rate during hyperinsulinemia, was milder in offspring of semistarved rats (O-SR) than in offspring of diabetic rats (O-DR). The basal GMI did not differ among the three groups in any tissue except tibialis anterior; during hyperinsulinemia, GMI was significantly greater in the insulin-sensitive tissues of all three groups. GMI of skeletal muscles and adipose tissue during hyperinsulinemia did not differ between control rats and O-SR; in contrast, the GMI was 25-50% lower in skeletal muscles of O-DR during hyperinsulinemia than in those of control rats or O-SR. Thus, maternal semistarvation and diabetes have dissimilar effects on peripheral insulin sensitivity of the adult female offspring. Because both conditions are associated with perinatal growth retardation and fetal hypoinsulinemia, other mechanisms must be identified to explain impaired glucose uptake by skeletal mucles in the offspring of diabetic rats.