Telles Mônica Marques, da Silva Thaís Girão, Watanabe Regina Lúcia Harumi, de Andrade Iracema Senna, Estadella Debora, Nascimento Cláudia Maria Oller, Oyama Lila Missae, Ribeiro Eliane Beraldi
Departamento de Fisiologia, Disciplina de Fisiologia da Nutrição, Universidade Federal de São Paulo (UNIFESP), São Paulo/SP, Brazil.
Regul Pept. 2013 Jun 10;184:75-80. doi: 10.1016/j.regpep.2013.03.027. Epub 2013 Mar 19.
Whether leptin targets the hypothalamic serotonergic system to inhibit food intake is not established. We examined the effect of a short-term i.c.v. leptin treatment on serotonin microdialysate levels in rat lateral hypothalamus. Adipose tissue gene expression was also evaluated. Male rats received four daily injections of leptin (5 μg) or vehicle (with pair-feeding to leptin-induced intake) and a fifth injection during collection of LH microdialysates. We found that serotonin and 5-HIAA levels were not affected by the leptin pre-treatment, as basal levels were similar between the leptin and the pair-fed group. These levels remained unaltered after the acute leptin injection. For gene expression studies, rats were pre-treated with five daily injections of either leptin (5 μg) or vehicle (with either pair-feeding or ad libitum intake). mRNA levels of resistin, adiponectin, lipoprotein lipase, and PPAR-gamma were unaltered by either leptin or pair-feeding. Leptin gene expression was significantly reduced by leptin but not by pair-feeding, in both the retroperitoneal (-74%) and the epididymal (-99%) depots while no differences were observed in the subcutaneous depot. The observations confirmed the absence of an acute stimulatory effect of central leptin on serotonin release in the lateral hypothalamus and showed that the pre-treatment with leptin failed to modify this pattern. This indicates that components of the serotonergic system are probably not directly affected by leptin. Additionally, the central effect of leptin was able to downregulate its own adipose tissue gene expression in a depot-specific manner while other adipokine genes were not affected.
瘦素是否通过作用于下丘脑5-羟色胺能系统来抑制食物摄入尚未明确。我们研究了短期脑室内注射瘦素对大鼠外侧下丘脑5-羟色胺微透析液水平的影响。同时也评估了脂肪组织的基因表达。雄性大鼠每日接受4次瘦素（5μg）注射或溶剂注射（并与瘦素诱导的摄入量进行配对喂养），在收集外侧下丘脑微透析液期间进行第5次注射。我们发现，瘦素预处理并未影响5-羟色胺和5-羟吲哚乙酸水平，因为瘦素组和配对喂养组的基础水平相似。急性注射瘦素后这些水平保持不变。对于基因表达研究，大鼠每日接受5次瘦素（5μg）或溶剂注射预处理（采用配对喂养或自由进食）。抵抗素、脂联素、脂蛋白脂肪酶和过氧化物酶体增殖物激活受体γ的mRNA水平不受瘦素或配对喂养的影响。瘦素可显著降低腹膜后（-74%）和附睾（-99%）脂肪库中的瘦素基因表达，但配对喂养则无此作用，而皮下脂肪库未观察到差异。这些观察结果证实了中枢性瘦素对外侧下丘脑5-羟色胺释放无急性刺激作用，并表明瘦素预处理未能改变这种模式。这表明5-羟色胺能系统的组成部分可能不受瘦素直接影响。此外，瘦素的中枢作用能够以脂肪库特异性方式下调其自身在脂肪组织中的基因表达，而其他脂肪因子基因则不受影响。
