首页> 外文期刊>The Journal of Physiology >Maternal taurine supplementation in the late pregnant rat stimulates postnatal growth and induces obesity and insulin resistance in adult offspring.
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Maternal taurine supplementation in the late pregnant rat stimulates postnatal growth and induces obesity and insulin resistance in adult offspring.

机译:在晚期妊娠大鼠中补充母体牛磺酸会刺激产后生长,并导致成年后代肥胖和胰岛素抵抗。

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An adequate supply of taurine during fetal life is important for normal beta-cell development and insulin action. An altered availability of taurine may programme glucose metabolism in utero and result in type 2 diabetes in adult age. We examined whether maternal taurine supplementation in late pregnant rats affects postnatal growth, adult body composition, insulin sensitivity and endogenous insulin secretion in intrauterine growth restricted (IUGR) and normal offspring. Uterine artery ligation or sham operations were performed on gestational day (GD) 19. Taurine supplementation was given to half of the dams from GD 18 until term, resulting in four groups of offspring: sham (n = 22), sham/taurine (n = 22), IUGR (n = 22) and IUGR/taurine (n = 24). The offspring were studied at 12 weeks of age. In offspring with normal birth weight, fetal taurine supplementation markedly stimulated postnatal growth. In sham/taurine females, fat depots, plasma free fatty acid and leptin concentrations were increased, and insulin sensitivity was reduced. Insulin sensitivity was unaltered in IUGR and IUGR/taurine offspring. However, whereas IUGR offspring showed little catch-up growth, 50% of IUGR/taurine animals displayed complete catch-up at 12 weeks of age, and these animals had increased fat depots and reduced insulin sensitivity. In conclusion, taurine supplementation in late gestation resulted in accelerated postnatal growth, which was associated with adult obesity and insulin resistance in both IUGR and normal offspring. This effect was particularly evident in females. These data suggest that fetal taurine availability is an important determinant for postnatal growth, insulin sensitivity and fat accumulation.
机译:胎儿期间牛磺酸的充足供应对于正常的β细胞发育和胰岛素作用很重要。牛磺酸可用性的改变可能会导致子宫内的葡萄糖代谢受到控制,并导致成年后患上2型糖尿病。我们检查了晚期妊娠大鼠中补充牛磺酸是否会影响宫内生长受限(IUGR)和正常后代的出生后生长,成年人体组成,胰岛素敏感性和内源性胰岛素分泌。在妊娠第19天进行子宫动脉结扎或假手术。从18 GD到足月,对一半水坝补充牛磺酸,形成四组后代:假(n = 22),假/牛磺酸(n = 22),IUGR(n = 22)和IUGR /牛磺酸(n = 24)。对后代进行了12周龄的研究。在具有正常出生体重的后代中,补充牛磺酸可显着刺激出生后的生长。在假/牛磺酸雌性动物中,脂肪堆积,血浆游离脂肪酸和瘦素浓度增加,胰岛素敏感性降低。 IUGR和IUGR /牛磺酸后代的胰岛素敏感性未改变。但是,尽管IUGR后代几乎没有追赶生长,但50%的IUGR /牛磺酸动物在12周龄时完全追赶,这些动物的脂肪库增加,胰岛素敏感性降低。总之,在妊娠后期补充牛磺酸可加速产后生长,这与成年肥胖和IUGR和正常后代的胰岛素抵抗有关。这种作用在女性中尤为明显。这些数据表明胎儿牛磺酸的可用性是决定出生后生长,胰岛素敏感性和脂肪积累的重要因素。

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