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Accretion of visceral fat and hepatic insulin resistance in pregnant rats

机译:妊娠大鼠内脏脂肪和肝胰岛素抵抗的增加

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First published Dec 11, 2007; doi:10.1152/ajpendo.00570.2007.-Insulin resistance (IR) is a hallmark of pregnancy. Because increased visceral fat (VF) is associated with IR in nonpregnant states, we reasoned that fat accretion might be important in the development of IR during pregnancy. To determine whether VF depots increase in pregnancy and whether VF contributes to IR, we studied three groups of 6-mo-old female Sprague-Dawley rats: 1) nonpregnant sham-operated rats (Nonpreg; n = 6), 2) pregnant sham-operated rats (Preg; n = 6), and 3) pregnant rats in which VF was surgically removed 1 mo before mating (PVF-; n = 6). VF doubled by day 19 of pregnancy (Nonpreg 5.1 +- 0.3, Preg 10.0 +- 1.0 g, P < 0.01), and PVF- had similar amounts of VF compared with Nonpreg (PVF- 4.6 +- 0.8 g). Insulin sensitivity was measured by riyperinsulinemic-euglycemic clamp in late gestation in chronically catheterized unstressed rats. Glucose IR (mg kg~(-1) min~(-1)) was highest in Nonpreg (19.4 +- 2.0), lowest in Preg (11.1 +- 1.4), and intermediate in PVF- (14.7 +- 0.6; P < 0.001 between all groups). During the clamp, Nonpreg had greater hepatic insulin sensitivity man Preg [hepatic glucose production (HGP): Nonpreg 4.5 +- 1.3, Preg 9.3 +- 0.5 mg-kg-min~(-1); P < 0.001]. With decreased VF, hepatic insulin sensitivity was similar to nonpregnant levels in PVF- (HGP 4.9 +- 0.8 mg-kg~(-1) min~(-1)). Both pregnant groups had lower peripheral glucose uptake compared with Nonpreg. In parallel with hepatic insulin sensitivity, hepatic triglyceride content was increased in pregnancy (Nonpreg 1.9 +- 0.4 vs. Preg 3.2 +- 0.3 mg/g) and decreased with removal of VF (PVF- 1.3 +- 0.4 mg/g; P < 0.05). Accretion of visceral fat is an important component in the development of hepatic IR in pregnancy, and accumulation of hepatic triglycerides is a mechanism by which visceral fat may modulate insulin action in pregnancy.
机译:首次发布于2007年12月11日; doi:10.1152 / ajpendo.00570.2007.-胰岛素抵抗(IR)是怀孕的标志。因为在非怀孕状态下内脏脂肪(VF)的增加与IR相关,因此我们认为脂肪积聚在怀孕期间IR的发展中可能很重要。为了确定妊娠中VF库是否增加以及VF是否对IR起作用,我们研究了三组6个月大的Sprague-Dawley雌性大鼠:1)未怀孕的假手术大鼠(Nonpreg; n = 6),2)怀孕的假手术-操作的大鼠(Preg; n = 6),和3)妊娠大鼠,其中在交配前1个月通过手术去除了VF(PVF-; n = 6)。在怀孕第19天时,VF翻了一番(Nonpreg 5.1 +-0.3,Preg 10.0 +-1.0 g,P <0.01),PVF-的VF量与Nonpreg(PVF- 4.6 +-0.8 g)相近。在慢性导管未压大鼠的妊娠晚期,通过riyperinsulinemic-euglycemic钳测量胰岛素敏感性。葡萄糖IR(mg kg〜(-1)min〜(-1))在Nonpreg中最高(19.4 +-2.0),在Preg中最低(11.1 +-1.4),在PVF-中最低(14.7 +-0.6; P所有组之间<0.001)。在钳夹期间,Nonpreg对肝脏的胰岛素敏感性高于Preg [肝葡萄糖生成(HGP):Nonpreg 4.5±1.3,Preg 9.3±0.5 mg-kg-min〜(-1); P <0.001]。随着VF的降低,肝胰岛素敏感性与PVF-中的非妊娠水平相似(HGP 4.9 +-0.8 mg-kg〜(-1)min〜(-1))。与Nonpreg相比,两个怀孕组的外周葡萄糖摄入量均较低。与肝胰岛素敏感性同时,妊娠期肝甘油三酸酯含量增加(非preg 1.9 +-0.4 vs. Preg 3.2 +-0.3 mg / g),并随着VF的去除而降低(PVF- 1.3 +-0.4 mg / g; P < 0.05)。内脏脂肪的积累是妊娠肝IR发展的重要组成部分,而肝甘油三酸酯的积累是内脏脂肪可能调节妊娠胰岛素作用的机制。

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