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Effects of exogenous insulin or vanadate on disposal of dietary triacylglycerols between mammary gland and adipose tissue in the lactating rat: insulin resistance in white adipose tissue.

机译:外源胰岛素或钒酸盐对泌乳大鼠乳腺和脂肪组织之间饮食中三酰甘油的处置的影响:白色脂肪组织中的胰岛素抵抗。

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摘要

The effects of exogenous insulin or vanadate (an insulin mimetic) on the disposal of dietary [14C]lipid between oxidation to 14CO2, deposition in adipose tissue or uptake by mammary gland and transfer to suckling pups were studied in virgin and lactating rats. After an oral load of [1-14C]triolein, virgin rats treated with a supraphysiological dose of insulin over 24 h showed a decrease (58%) in 14CO2 production and increased accumulation of [14C]lipid in carcass and white adipose tissue. There was a 2.5-fold increase in lipoprotein lipase activity in the latter. Chronic vanadate administration (12 days) had no effect on these parameters. In lactating rats, the stimulation of the deposition of [14C]lipid in adipose tissue by exogenous insulin was about 10% of that in virgin rats. In prolactin-deficient lactating rats there was no stimulation of [14C]lipid deposition in adipose tissue by insulin. However, both insulin and vanadate treatment increased the accumulation of [14C]lipid in mammary gland to the values seen in the mammary glands plus pups of normal lactating rats. Lipoprotein lipase activity in the gland was also restored to normal values. It is concluded that in lactation there is resistance to insulin stimulation of dietary lipid deposition in adipose tissue, and that this is not due to circulating prolactin. In addition, exogenous insulin plays a role in the regulation of lipoprotein lipase and hence of dietary lipid uptake into lactating mammary gland.
机译:在处女和哺乳期大鼠中,研究了外源胰岛素或钒酸盐(胰岛素模拟物)对饮食中[14C]脂质的氧化,氧化成14CO2,沉积在脂肪组织中或被乳腺摄取以及转移至乳仔中的作用。口服[1-14C]三油精后,经超生理学剂量的胰岛素治疗的原始大鼠在24小时内显示14CO2产生减少(58%),[体和白色脂肪组织中[14C]脂质的积累增加。后者的脂蛋白脂酶活性增加了2.5倍。长期服用钒酸盐(12天)对这些参数没有影响。在哺乳期大鼠中,外源性胰岛素对脂肪组织中[14C]脂质沉积的刺激约为原始大鼠的10%。在泌乳素不足的哺乳期大鼠中,胰岛素没有刺激脂肪组织中的[14C]脂质沉积。但是,胰岛素和钒酸盐处理均会增加[14C]脂质在乳腺中的蓄积,使其达到在正常泌乳大鼠的乳腺和幼崽中所见的值。腺体中脂蛋白脂肪酶的活性也恢复到正常值。可以得出结论,在泌乳期,胰岛素刺激饮食中脂肪组织中的饮食脂质沉积,并且这不是由于循环催乳激素引起的。另外,外源胰岛素在脂蛋白脂酶的调节中起作用,因此在饮食中脂类摄入到乳腺中也起作用。

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