Meister B, Arvidsson U
institutionen för neurovetenskap, Karolinska institutet, Stockholm.
Lakartidningen. 1996 Jan 24;93(4):247-51.
The existence of mice (ob/ob mice) with a genetic defect causing obesity and type II diabetes has been known since 1950. The mutated ob gene was recently identified and characterized. The gene encodes a 167 amino acid protein that has been given the name leptin, from the greek word leptos, meaning thin. The functionally active hormone, which is synthesised and secreted by adipocytes, is lacking in homozygote ob/ob mice, causing an increase in body fat. Injection of recombinant leptin in ob/ob mice induces loss of fat due to decreased appetite and increased energy expenditure. The ob gene product leptin acts via binding sites in the hypothalamus, where the centre for appetite and satiety is located. Research is now focused on the identification, characterization and cloning of leptin-receptors. Other mice, also with a genetic defect causing obesity and type II diabetes, do not respond to leptin treatment and are therefore suspected to have defective leptin receptors.
自1950年以来,人们就知道存在一种因基因缺陷导致肥胖和II型糖尿病的小鼠(ob/ob小鼠)。最近,突变的ob基因已被鉴定和表征。该基因编码一种167个氨基酸的蛋白质,它被命名为瘦素,来源于希腊语leptos,意为瘦。这种功能活跃的激素由脂肪细胞合成和分泌,纯合子ob/ob小鼠缺乏这种激素,导致体脂增加。给ob/ob小鼠注射重组瘦素会因食欲下降和能量消耗增加而导致脂肪减少。ob基因产物瘦素通过位于下丘脑的食欲和饱腹感中枢的结合位点发挥作用。目前的研究集中在瘦素受体的鉴定、表征和克隆上。其他同样因基因缺陷导致肥胖和II型糖尿病的小鼠对瘦素治疗没有反应,因此怀疑它们的瘦素受体存在缺陷。