RT Journal Article
SR Electronic
T1 POMC-specific knockdown of Tril reduces body adiposity and increases hypothalamic leptin responsiveness
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2020.06.25.172379
DO 10.1101/2020.06.25.172379
A1 Moura-Assis, Alexandre
A1 Nogueira, Pedro A.
A1 de-Lima-Junior, Jose C.
A1 Simabuco, Fernando M.
A1 Gaspar, Joana M.
A1 Donato, Jose
A1 Velloso, Licio A.
YR 2020
UL http://biorxiv.org/content/early/2020/06/27/2020.06.25.172379.abstract
AB In a public dataset of transcripts differentially expressed in selected neuronal subpopulations of the arcuate nucleus, we identified TLR4-interactor with leucine-rich repeats (Tril) as a potential candidate for mediating the harmful effects of a high-fat diet in proopiomelanocortin (POMC) neurons. The non-cell-specific inhibition of Tril in the arcuate nucleus resulted in reduced hypothalamic inflammation, protection against diet-induced obesity associated with increased whole-body energy expenditure and increased systemic glucose tolerance. The inhibition of Tril, specifically in POMC neurons, resulted in a trend for protection against diet-induced obesity, increased energy expenditure and increased hypothalamic sensitivity to leptin. Thus, Tril emerges as a new component of the complex mechanisms that promote hypothalamic dysfunction in experimental diet-induced obesity.Competing Interest StatementThe authors have declared no competing interest.