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Diet-induced adaptive thermogenesis requires neuropeptide FF receptor-2 signalling

Zhang, L.; Ip, C.Kin.; Lee, I-Chieh.J.; Qi, Y.; Reed, F.; Karl, T.; Low, J.Kee.; Enriquez, R.F.; Lee, N.J.; Baldock, P.A.; Herzog, H.

Nature Communications 9(1): 4722

2018


ISSN/ISBN: 2041-1723
PMID: 30413707
DOI: 10.1038/s41467-018-06462-0
Accession: 071590791

Excess caloric intake results in increased fat accumulation and an increase in energy expenditure via diet-induced adaptive thermogenesis; however, the underlying mechanisms controlling these processes are unclear. Here we identify the neuropeptide FF receptor-2 (NPFFR2) as a critical regulator of diet-induced thermogenesis and bone homoeostasis. Npffr2-/- mice exhibit a stronger bone phenotype and when fed a HFD display exacerbated obesity associated with a failure in activating brown adipose tissue (BAT) thermogenic response to energy excess, whereas the activation of cold-induced BAT thermogenesis is unaffected. NPFFR2 signalling is required to maintain basal arcuate nucleus NPY mRNA expression. Lack of NPFFR2 signalling leads to a decrease in BAT thermogenesis under HFD conditions with significantly lower UCP-1 and PGC-1α levels in the BAT. Together, these data demonstrate that NPFFR2 signalling promotes diet-induced thermogenesis via a novel hypothalamic NPY-dependent circuitry thereby coupling energy homoeostasis with energy partitioning to adipose and bone tissue.

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