Holst J J
Medicinsk Fysiologisk Institut, Københavns Universitet, Panum-instituttet.
Nord Med. 1996 Nov;111(9):300-3.
The relatively constant level of body fat in the adult mammal is explained by the lipostat theory as follows: A factor is released from adipose tissue in amounts that reflect total body fat content. This factor is then registered by the hypothalamic centres that regulate appetite. The theory has gained particular support from parabiotic experiments in genetically fat mice, amongst whom the so-called ob/ob mice appear to produce too little of the factor, whilst signal transduction to the satiety centre appears to be defective in the so-called db/db mice. The two genetic defects have recently been clarified, and it has been shown that the normal ob gene nodes for a protein called leptin. Leptin is released from adipose tissue, and its plasma concentration reflects total body fat. The normal db-gene codes for a hypothalamic receptor for leptin. These crucial discoveries have greatly supported the correctness of the lipostat theory. At present, extensive investigations of the roles of leptin and the leptin receptor in human adiposity are in progress.
成年哺乳动物体内脂肪水平相对恒定，根据脂肪稳态理论可解释如下：一种因子从脂肪组织中释放出来，其释放量反映了全身脂肪含量。然后，该因子被调节食欲的下丘脑中枢所记录。该理论从对遗传性肥胖小鼠的联体实验中获得了特别的支持，在这些小鼠中，所谓的ob/ob小鼠似乎产生的这种因子过少，而在所谓的db/db小鼠中，向饱足中枢的信号转导似乎存在缺陷。最近，这两种基因缺陷已被阐明，结果表明正常的ob基因编码一种名为瘦素的蛋白质。瘦素从脂肪组织中释放出来，其血浆浓度反映了全身脂肪情况。正常的db基因编码一种下丘脑瘦素受体。这些重要发现极大地支持了脂肪稳态理论的正确性。目前，关于瘦素和瘦素受体在人类肥胖症中作用的广泛研究正在进行。
