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

Lei Zhang, Chi Kin Ip, I-Chieh J. Lee, Yue Qi, Felicia Reed, Tim Karl, Jac Kee Low, Ronaldo F. Enriquez, Nicola J. Lee, Paul A. Baldock and Herbert Herzog ()
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Lei Zhang: Garvan Institute of Medical Research, St. Vincent’s Hospital
Chi Kin Ip: Garvan Institute of Medical Research, St. Vincent’s Hospital
I-Chieh J. Lee: Garvan Institute of Medical Research, St. Vincent’s Hospital
Yue Qi: Garvan Institute of Medical Research, St. Vincent’s Hospital
Felicia Reed: Garvan Institute of Medical Research, St. Vincent’s Hospital
Tim Karl: Western Sydney University
Jac Kee Low: Neuroscience Research Australia
Ronaldo F. Enriquez: Garvan Institute of Medical Research, St. Vincent’s Hospital
Nicola J. Lee: Garvan Institute of Medical Research, St. Vincent’s Hospital
Paul A. Baldock: University of NSW
Herbert Herzog: Garvan Institute of Medical Research, St. Vincent’s Hospital

Nature Communications, 2018, vol. 9, issue 1, 1-19

Abstract: Abstract 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.

Date: 2018
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DOI: 10.1038/s41467-018-06462-0

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