Konturek P C, Konturek S J, Brzozowski T, Jaworek J, Hahn E G
Department of Medicine, University of Erlangen-Nuremberg, Erlangen, Germany.
J Physiol Paris. 2001 Jan-Dec;95(1-6):345-54. doi: 10.1016/s0928-4257(01)00047-x.
Leptin, a 16 kDa protein encoded by the ob gene, is known mainly for its role in the regulation of food intake, body composition and energy expenditure through a central feedback mechanism. Initially leptin was considered as an ob gene product of adipocytes but recently the presence of leptin and its receptors have been revealed in other organs including gastric mucosa and the pancreas and found to be released from these organs by cholecystokinin (CCK), gastrin and ordinary feeding. Furthermore, leptin was found to mimic the action of CCK on gastric and pancreatic integrity, while reducing the food intake and to affect gastric and pancreatic secretion. This report emphasizes the role of leptin originating from the gastrointestinal tract acting synergistically with CCK at the hypothalamus level on the mechanism of food intake and locally on the protection of gastric mucosa and the pancreas against noxious agents and to maintain tissue integrity.
瘦素是一种由ob基因编码的16 kDa蛋白质,主要通过中枢反馈机制在调节食物摄入、身体组成和能量消耗方面发挥作用。最初,瘦素被认为是脂肪细胞的ob基因产物,但最近在包括胃黏膜和胰腺在内的其他器官中发现了瘦素及其受体,并发现它们通过胆囊收缩素(CCK)、胃泌素和正常进食从这些器官释放出来。此外,发现瘦素可模拟CCK对胃和胰腺完整性的作用,同时减少食物摄入,并影响胃和胰腺分泌。本报告强调了源自胃肠道的瘦素在下丘脑水平与CCK协同作用于食物摄入机制,并在局部对胃黏膜和胰腺起到保护作用,使其免受有害物质侵害并维持组织完整性。