Sucajtys-Szulc Elzbieta, Goyke Elzbieta, Korczynska Justyna, Stelmanska Ewa, Rutkowski Boleslaw, Swierczynski Julian
Department of Nephrology, Transplantology and Internal Medicine, Medical University of Gdansk, 80-211 Gdansk, Poland.
Neuropeptides. 2009 Aug;43(4):321-5. doi: 10.1016/j.npep.2009.05.001. Epub 2009 Jun 18.
Rat adipose tissue is the principal site of leptin synthesis, however, leptin gene expression has been demonstrated in many rat tissues. Some data indicate that leptin produced by human brain and adipose tissue could cooperate in the regulation of food intake. In this case the regulation of leptin gene expression in hypothalamus and in adipose tissue should be coordinately regulated. Food restriction is often undertaken by many humans trying to lose body weight. Thus, the current study was aimed to analyze whether leptin gene expression in rat hypothalamus and in adipose tissue is regulated synchronously by prolonged food restriction and prolonged food restriction/refeeding. We demonstrate here that although leptin gene is expressed at very low level in rat hypothalamus, its expression in hypothalamus was down-regulated by prolonged food restriction similarly as in the white adipose tissue. Refeeding after prolonged food restriction caused both an increase of leptin gene expression in white adipose tissue and the increase in serum leptin concentration. In contrast, no significant effect of prolonged food restriction/refeeding on hypothalamic leptin gene expression was observed. The reduction of leptin gene expression in both hypothalamus and white adipose tissue by prolonged food restriction was associated with a significant increase of NPY gene (a target of leptin signaling) expression in hypothalamus. Refeeding after prolonged food restriction caused the decrease of NPY gene expression in hypothalamus, however NPY mRNA level remained higher than in controls. The results presented in this paper indicate that prolonged food restriction/refeeding differentially affects leptin gene expression in adipose tissue and in hypothalamus. Moreover, obtained data suggest that in rats leptin synthesized in hypothalamus exerts marginal effect on NPY gene expression and on serum leptin concentration.
大鼠脂肪组织是瘦素合成的主要部位,然而,已证实在许多大鼠组织中都有瘦素基因表达。一些数据表明,人脑和脂肪组织产生的瘦素可能共同参与食物摄入的调节。在这种情况下,下丘脑和脂肪组织中瘦素基因表达的调节应该是协同进行的。许多试图减肥的人常常会进行节食。因此,本研究旨在分析长期节食以及长期节食/再喂食是否会同步调节大鼠下丘脑和脂肪组织中的瘦素基因表达。我们在此证明,尽管瘦素基因在大鼠下丘脑中的表达水平非常低,但与白色脂肪组织一样,长期节食会使其在下丘脑中的表达下调。长期节食后的再喂食导致白色脂肪组织中瘦素基因表达增加以及血清瘦素浓度升高。相反,未观察到长期节食/再喂食对下丘脑瘦素基因表达有显著影响。长期节食使下丘脑和白色脂肪组织中的瘦素基因表达降低,这与下丘脑NPY基因(瘦素信号传导的一个靶点)表达显著增加有关。长期节食后的再喂食导致下丘脑NPY基因表达降低,然而NPY mRNA水平仍高于对照组。本文给出的结果表明,长期节食/再喂食对脂肪组织和下丘脑的瘦素基因表达有不同影响。此外,所得数据表明,在大鼠中,下丘脑合成的瘦素对NPY基因表达和血清瘦素浓度的影响很小。