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首页> 外文期刊>The journal of maternal-fetal & neonatal medicine >Basal, endogenous leptin is metabolically active in newborn rat pups
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Basal, endogenous leptin is metabolically active in newborn rat pups

机译:新生大鼠幼鼠的基础内源性瘦素具有代谢活性

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Objective.The adipocyte-derived hormone leptin regulates food intake and body weight via the activation of JAK-STAT pathway in mammalian adult hypothalamic neurons. To investigate whether endogenous leptin is metabolically active in newborn rat pups, the JAK-STAT leptin signaling pathway was analyzed following leptin antagonist challenge. Methods.One day old male control pups were injected with either (i) saline, (ii) leptin (10μg/g, s.c; n=4), (iii) pegylated leptin antagonist (PEG-MLA, 20μg/g, s.c, n=4), or (iv) leptin plus PEG-MLA. Hypothalamus was dissected from individual pups at 30, 45, and 60min. Protein expression of ObR, STAT3, pSTAT3, and SOCS3 was analyzed by Western blot. Results.Leptin, but not PEG-MLA, produced a significant increase in hypothalamic pSTAT3 relative to saline treatment. Systemically administered PEG-MLA effectively blocks leptin signal induction of hypothalamic JAK-STAT signaling. The presence of PEG-MLA in combination with leptin attenuated the leptin-induced increase in pSTAT3. Conclusions.Thus, basal leptin levels are metabolically active in the newborn rats. These results brings new insights in considering the importance of endogenous leptin at birth, especially in low birth weight offspring who may be predisposed to altered neurogenesis and later obesity, and provide potential therapeutic strategies for programmed or diet-induced obesity.
机译:脂肪细胞源性激素瘦素通过激活成年下丘脑神经元的JAK-STAT途径调节食物摄入和体重。为了研究内源性瘦素在新生大鼠幼崽中是否具有代谢活性,在瘦素拮抗剂攻击后分析了JAK-STAT瘦素信号传导途径。方法:给一天大的雄性对照幼犬注射(i)盐水,(ii)瘦素(10μg/ g,sc; n = 4),(iii)聚乙二醇化的瘦素拮抗剂(PEG-MLA,20μg/ g,sc, n = 4),或(iv)瘦素加PEG-MLA。在30、45和60分钟时从各只幼崽解剖下丘脑。通过蛋白质印迹分析ObR,STAT3,pSTAT3和SOCS3的蛋白表达。结果:相对于盐水治疗,瘦素而非PEG-MLA引起下丘脑pSTAT3的显着增加。全身施用的PEG-MLA有效阻止下丘脑JAK-STAT信号传导的瘦素信号诱导。 PEG-MLA与瘦素结合的存在减弱了瘦素诱导的pSTAT3增加。结论:因此,新生大鼠的基础瘦素水平具有代谢活性。这些结果为考虑内源性瘦素在出生时的重要性提供了新的见识,尤其是在低出生体重的后代中,后者可能倾向于改变神经发生和后来的肥胖症,并为程序性或饮食性肥胖症提供了潜在的治疗策略。

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