The leptin (OB-R) receptor is a member of the cytokine receptor superfamily which plays an important role in mammalian body weight homeostasis and energy balance. Ligand-induced activation of the OB-R by the adipose tissue-secreted hormone, leptin, appears to activate downstream signaling events through the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway. Leptin can homo-dimerize OB-R extracellular domains while downstream signaling events are initiated upon homo-dimerization of OB-R intracellular domains. Several isoforms of the OB-R which differ in length and signaling capabilities have been reported. RNA transcripts encoding the OB-R long form have been found in the choroid plexus and in the hypothalamus which has been proposed as a control center for satiety and energy expenditure. Mutations in either the mouse OB-R (db) or leptin (ob) genes have been shown to result in early-onset obesity. Metabolic abnormalities attributable to these genotypes include hypercorticoidemia, hyperinsulinemia and insulin resistance, hyperglycemia, altered CNS activity, reduced metabolic rate of brown adipose tissue, and a large increase in white adipose tissue.
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Protein Aliases: B219; CD antigen CD295; CD295; CD295 antigen; HuB219; HuB219.2; LEP-R; Leptin receptor; Leptin receptor (fatty); leptin receptor gene-related protein; OB receptor; OB-R
Gene Aliases: CD295; DB; diabetes; Fa; LEP-R; LEPR; Leprb; LEPRD; LEPROT; Modb1; OB-R; OB-RGRP; obese-like; obl; OBR