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2018 ; 8
(1
): 11001
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Sympathetic inputs regulate adaptive thermogenesis in brown adipose tissue
through cAMP-Salt inducible kinase axis
#MMPMID30030465
Paulo E
; Wu D
; Wang Y
; Zhang Y
; Wu Y
; Swaney DL
; Soucheray M
; Jimenez-Morales D
; Chawla A
; Krogan NJ
; Wang B
Sci Rep
2018[Jul]; 8
(1
): 11001
PMID30030465
show ga
Various physiological stimuli, such as cold environment, diet, and hormones,
trigger brown adipose tissue (BAT) to produce heat through sympathetic nervous
system (SNS)- and ?-adrenergic receptors (?ARs). The ?AR stimulation increases
intracellular cAMP levels through heterotrimeric G proteins and adenylate
cyclases, but the processes by which cAMP modulates brown adipocyte function are
not fully understood. Here we described that specific ablation of cAMP production
in brown adipocytes led to reduced lipolysis, mitochondrial biogenesis,
uncoupling protein 1 (Ucp1) expression, and consequently defective adaptive
thermogenesis. Elevated cAMP signaling by sympathetic activation inhibited
Salt-inducible kinase 2 (Sik2) through protein kinase A (PKA)-mediated
phosphorylation in brown adipose tissue. Inhibition of SIKs enhanced Ucp1
expression in differentiated brown adipocytes and Sik2 knockout mice exhibited
enhanced adaptive thermogenesis at thermoneutrality in an Ucp1-dependent manner.
Taken together, our data indicate that suppressing Sik2 by PKA-mediated
phosphorylation is a requisite for SNS-induced Ucp1 expression and adaptive
thermogenesis in BAT, and targeting Sik2 may present a novel therapeutic strategy
to ramp up BAT thermogenic activity in humans.
|Adipose Tissue, Brown/*physiology
[MESH]
|Animals
[MESH]
|Cyclic AMP-Dependent Protein Kinases/metabolism
[MESH]