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Transcriptional and physiological roles for STAT proteins in leptin action.
Authors Pan W, Allison MB, Sabatini P, Rupp A, Adams J, Patterson C, Jones JC, Olson DP,
Myers MG
Submitted By Submitted Externally on 5/13/2019
Status Published
Journal Molecular metabolism
Year 2019
Date Published 4/1/2019
Volume : Pages 22 : 121 - 131
PubMed Reference 30718218
Abstract Leptin acts via its receptor LepRb on specialized neurons in the brain to
modulate food intake, energy expenditure, and body weight. LepRb activates
signal transducers and activators of transcription (STATs, including STAT1,
STAT3, and STAT5) to control gene expression., Because STAT3 is crucial for
physiologic leptin action, we used TRAP-seq to examine gene expression in LepRb
neurons of mice ablated for Stat3 in LepRb neurons (Stat3LepRbKO mice),
revealing the STAT3-dependent transcriptional targets of leptin. To understand
roles for STAT proteins in leptin action, we also ablated STAT1 or STAT5 from
LepRb neurons and expressed a constitutively-active STAT3 (CASTAT3) in LepRb
neurons., While we also found increased Stat1 expression and STAT1-mediated
transcription of leptin-regulated genes in Stat3LepRbKO mice, ablating Stat1 in
LepRb neurons failed to alter energy balance (even on the Stat3LepRbKO
background); ablating Stat5 in LepRb neurons also failed to alter energy
balance. Importantly, expression of a constitutively-active STAT3 (CASTAT3) in
LepRb neurons decreased food intake and body weight and improved metabolic
parameters in leptin-deficient (ob/ob) mice, as well as in wild-type animals.,
Thus, STAT3 represents the unique STAT protein required for leptin action and
STAT3 suffices to mediate important components of leptin action in the absence
of other LepRb signals.


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