Functional STAT 1 and 3 signaling by the leptin receptor (OB-R); reduced expression of the rat fatty leptin receptor in transfected cells

• Published in: Endocrinology (Philadelphia) 1996-11, Vol.137 (11), p.5178-5181
• Main Authors: Rosenblum, C I, Tota, M, Cully, D, Smith, T, Collum, R, Qureshi, S, Hess, J F, Phillips, M S, Hey, P J, Vongs, A, Fong, T M, Xu, L, Chen, H Y, Smith, R G, Schindler, C, Van der Ploeg, L H
• Format: Article
• Language: English
• Subjects: Animals; Base Sequence; Carrier Proteins - biosynthesis; Carrier Proteins - physiology; Cell Line; COS Cells; DNA Probes; DNA-Binding Proteins - metabolism; Homology; Hypothalamus - metabolism; Kinetics; Leptin; Low level; Mice; Obesity; Oligodeoxyribonucleotides; Phenotypes; Polymerase Chain Reaction; Proteins - metabolism; Proteins - pharmacology; Rats; Rats, Zucker; Receptors; Receptors, Cell Surface; Receptors, Leptin; Recombinant Proteins - biosynthesis; Signal Transduction; Stat1 protein; STAT1 Transcription Factor; Stat3 protein; STAT3 Transcription Factor; Trans-Activators - metabolism; Transfection
• ISSN: 0013-7227; 1945-7170
• DOI: 10.1210/endo.137.11.8895396

The leptin receptor (OB-R) bears homology to members of the class I cytokine receptor family. We demonstrate that leptin binding to OB-R stimulates formation of STAT-1 and STAT-3 complexes, thereby defining transcriptional motifs for genes that are under leptin control. Transfected fa OB-R bound leptin with equal affinity to that of wild type OB-R. fa OB-R abundance was about 7 fold reduced compared to control cells. Surprisingly, the low level of fa OB-R is fully capable of activating the STAT signal transduction pathway. We discuss plausible explanations for the obese phenotype in Zucker fatty rats.