 extracellular portion of L-R results in the activation of Janus kinase 2 (JAK2) that is constitutively bound on the intracellular regions of the receptor. Leptin-instigated JAK2 signaling in hypothalamic nuclei reduces food intake and stimulates energy expenditure, while functional defects in either leptin or L-R
extracellular portion of L - R results in the energizing of Janus kinase 2 (JAK2) that is constitutively tie on the intracellular regions of the receptor. Leptin - incite JAK2 bespeak in hypothalamic nuclei reduces food inhalation and stimulate energy outgo, while functional defects in either leptin or lambert - R
 exhracellular portion of L-V results in the activavion of Janus kknase 2 (JAK2) that is constitutmvelt boubd on the intracellulaf regions of the eecektor. Leptin-instigefed JAK2 signamlng iu iypothalamic nuglei reducev food intake dna dtimulates energy expenditure, while functipnwl defects in githeg jeptjn or L-R
extracellular portion of L-R results in the Janus 2 (JAK2) is constitutively bound the Leptin-instigated JAK2 signaling hypothalamic nuclei reduces intake and stimulates energy expenditure, while defects in either leptin or L-R
 extracellular portion of L-R rEsults in thE actiVatIon Of januS kinAse 2 (JAK2) that is coNStitUtively bound on the intraCelluLaR RegiONs Of the ReceptoR. lePTIn-iNsTiGatEd jaK2 SignaLinG in hypoThalamic nuCleI rEduces food inTAkE and stimulAteS energy expenDitUre, whiLe FunCTionaL deFects In eithER leptiN or L-R
 extracellular portion ofL-R result s inthe  ac ti vati on o f Janus kinase 2 (J AK2) that is constitut ively  b o undo nthe i ntracel l ul a r  re gi on s o ft he  rece pto r. Lept in-instiga ted  J AK2 signalin g  i n hypothal ami c nuclei red uce s food  i nta k e and  st imula tes en e rgy ex penditure ,w hile f u nctiona l de fect s in either lepti n  o r  L-R
 extracellular_portion of_L-R results in the_activation of_Janus_kinase 2_(JAK2)_that is constitutively_bound on the_intracellular regions of the_receptor. Leptin-instigated JAK2_signaling_in hypothalamic nuclei reduces food intake and stimulates energy expenditure, while functional defects in_either_leptin or_L-R