期刊
PEDIATRIC RESEARCH
卷 67, 期 2, 页码 138-143出版社
NATURE PUBLISHING GROUP
DOI: 10.1203/PDR.0b013e3181c2f4cc
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资金
- Ministry of Education, Culture, Sports, Science and Technology, Japan [15659393, 16390475, 17390450, 17591728, 17591730, 17659513, 18390446]
- Ministry of Health, Labor and Welfare
- Smoking Research Foundation
- Takeda Science Foundation
- Takeda Medical Research Foundation
- The Naito Foundation
- Uehara Memorial Foundation
- Food Science Institute Foundation
- Precursory Research for Embryonic Science and Technology (PRESTO)
- Japan Science and Technology Agency (JST)
- Grants-in-Aid for Scientific Research [15659393, 17591728, 18390446, 17390450, 17591730, 17659513, 16390475, 22591822] Funding Source: KAKEN
Glucose is a major fuel for fetal development. Fetal blood glucose level is mainly dependent on maternal blood glucose concentration, though it is also regulated by fetal insulin level. Thioredoxin binding protein-2 (TBP-2), which is identical to vitamin D3 up-regulated protein (VDUP1) and thioredoxin interacting protein (Txnip), was recently reported to be a key transcriptional factor controlling glucose metabolism. Here, we elucidated the functions of TBP-2 in maintaining blood glucose homeostasis during the fetal period. TBP-2(+/-) female mice were mated with TBP-2(+/-) male mice; beginning 16.5-d post coitum, pregnant mice were fed or fasted for 24 h. Under conditions of maternal starvation, the blood glucose levels of TBP-2(-/-) fetuses were significantly lower than those of TBP-2(+/+) fetuses, corresponding to the elevated plasma insulin levels of TBP-2(-/-) fetuses compared with those of TBP-2(+/+) fetuses. There was no difference between TBP-2(+/+) and TBP-2(-/-) fetuses in terms of their pancreatic P-cell masses or the expression of placental glucose transporters under conditions of either maternal feeding or fasting. Thus, during maternal fasting, fetal TBP-2 suppresses excessive insulin secretion to maintain the fetus's glucose levels, implying that TBP-2 is a critical molecule in mediating fetal glucose homeostasis depending on nutrient availability. (Pediatr Res 67: 138-143, 2010)
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