Macut D, Micić D
Institut za endokrinologiju, dijabetes i bolesti metabolizma, Klinicki centar Srbije, Beograd.
Med Pregl. 1998 Sep-Oct;51(9-10):410-4.
Leptin is a secretory product of adipocytes. It has been suggested that leptin acts as an afferent satiety signal to the brain modulating the expression of the orexigenic hypothalamic peptide, neuropeptide Y (NPY). Therefore leptin can be regarded as a marker of the nutritional status of the body. It was proposed that human obesity may result from a central resistance to leptin due to different pathophysiological mechanisms: saturation of the leptin transport into the cerebrospinal fluid of the obese subjects, abnormalities in the hypothalamic receptor for leptin, or post-receptor transduction mechanisms. It was shown that circulating leptin levels in humans significantly correlate with the body mass index (BMI). Although most studies point to white adipose tissue as a primary source of leptin there is still some uncertainty towards the relative expression of leptin between various body fat compartments. LEPTIN AND ONSET OF PUBERTY: Studies on animal models recognized various metabolic candidates for modulation of GnRH neuronal activity. It was supposed that mild changes in the body's metabolic status can serve to regulate the central drive to the reproductive axis. It is likely that leptin can serve as a "metabolic cue" that transmits signals of those mild metabolic changes towards activation of the GnRH neuronal system at the end of the prepubertal period. On the other side there is a possibility of altered leptin pulsatility during prepubertal period that can consequently influence hypothalamus and GnRH neuronal system. LEPTIN AND SEXUAL DIMORPHISM: Leptin levels in humans are similar in both sexes during the prepubertal period. During puberty leptin has a tendency to decline in boys and to remain constant in girls. Puberty is also characterized with a similar circadian rhythm pattern between sexes whil girls express different pulse characteristics. It seems that sexual dimorphism is established in early phases of human development. There is a possibility of sex steroid influence on such sexual dimorphism. LEPTIN AND REPRODUCTIVE FUNCTION: It was shown that administration of recombinant leptin to ob ob mice could restore fertility in these infertile animals. There is certain difference in leptin levels according to the phase of the menstrual cycle. It was shown that leptin peak is in the luteal phase of the cycle and that correlates to the maximal progesterone level. It is possible that leptin could directly influence ovary and that disruption of such an effect could play a role in menstrual irregularities in both obese and mal nourished women. This could even become a pathophysiological mechanism in women with polycystic ovary syndrome (PCOS). It was supposed that leptin resistance could be involved in infertility impairment of the obese women with PCOS. Leptin increases during pregnancy. Appearance of placenta as a new, nonadipose source of leptin production, increases a possibility of different leptin mRNA expression through gestation.
瘦素是脂肪细胞的一种分泌产物。有人提出，瘦素作为一种传入性饱腹感信号作用于大脑，调节下丘脑促食欲肽神经肽Y（NPY）的表达。因此，瘦素可被视为身体营养状况的一个标志物。有人提出，人类肥胖可能是由于不同的病理生理机制导致对瘦素产生中枢性抵抗：肥胖受试者脑脊液中瘦素转运饱和、下丘脑瘦素受体异常或受体后转导机制异常。研究表明，人类循环中的瘦素水平与体重指数（BMI）显著相关。尽管大多数研究指出白色脂肪组织是瘦素的主要来源，但对于不同身体脂肪部位之间瘦素的相对表达仍存在一些不确定性。
对动物模型的研究识别出了多种调节促性腺激素释放激素（GnRH）神经元活性的代谢候选物。据推测，身体代谢状态的轻微变化可用于调节对生殖轴的中枢驱动。瘦素很可能作为一种“代谢信号”，在青春期前期末期将这些轻微代谢变化的信号传递给GnRH神经元系统以激活它。另一方面，青春期前时期瘦素脉冲性可能发生改变，从而影响下丘脑和GnRH神经元系统。
青春期前男女的瘦素水平相似。青春期期间，男孩的瘦素水平有下降趋势，而女孩的瘦素水平保持不变。青春期的特征还包括男女之间有相似的昼夜节律模式，而女孩表现出不同的脉冲特征。似乎性别差异在人类发育的早期阶段就已确立。性类固醇有可能影响这种性别差异。
研究表明，给ob/ob小鼠注射重组瘦素可恢复这些不育动物的生育能力。根据月经周期的阶段，瘦素水平存在一定差异。研究表明，瘦素峰值出现在月经周期的黄体期，且与最大孕酮水平相关。瘦素可能直接影响卵巢，这种作用的破坏可能在肥胖和营养不良女性的月经不调中起作用。这甚至可能成为多囊卵巢综合征（PCOS）女性的一种病理生理机制。据推测，瘦素抵抗可能与PCOS肥胖女性的不孕障碍有关。孕期瘦素水平会升高。胎盘作为瘦素产生的一个新的非脂肪来源出现，增加了整个孕期不同瘦素mRNA表达的可能性。
