Stephens T W, Caro J F
Lilly Research Laboratories, Lilly Corporate Center, Indianapolis, Indiana 46285, USA.
Exp Clin Endocrinol Diabetes. 1998;106(1):1-15. doi: 10.1055/s-0029-1211943.
Leptin and the leptin receptor genes have been identified as the site of mutations in the peripheral adipocyte hormone pathway responsible for obesity in the ob/ob mouse (Zhang et al., 1994) and the db/db mouse (Chen et al., 1996). In obese humans, ob/ob like mutations in leptin are rare but confirm a role for leptin (Montague et al., 1997), and db/db like mutations in the leptin receptor have not been found (Considine et al., 1996a); however, the increased understanding of the molecular basis for obesity has generated tremendous interest among scientists and patients alike. The new knowledge could be the base for intelligent drugs for the treatment of obesity. Herein we will put in perspective a) the physiological background that led to the discovery of leptin, b) leptin biosynthesis, c) leptin action and d) the clinical issues related to leptin as a drug for the treatment of obesity.
瘦素及瘦素受体基因已被确定为外周脂肪细胞激素途径中的突变位点，该途径与ob/ob小鼠（张等人，1994年）和db/db小鼠（陈等人，1996年）的肥胖有关。在肥胖人类中，瘦素的ob/ob样突变很少见，但证实了瘦素的作用（蒙塔古等人，1997年），且尚未发现瘦素受体的db/db样突变（康西丁等人，1996年a）；然而，对肥胖分子基础的深入了解在科学家和患者中都引起了极大兴趣。这些新知识可能成为治疗肥胖的智能药物的基础。在此，我们将阐述以下内容：a）导致瘦素发现的生理背景，b）瘦素的生物合成，c）瘦素的作用，以及d）与瘦素作为治疗肥胖药物相关的临床问题。
