Diet-induced adaptive thermogenesis requires neuropeptide FF receptor-2 signalling
| Autor: | I-Chieh J. Lee, Chi Kin Ip, Paul A. Baldock, Jac Kee Low, Herbert Herzog, Ronaldo F. Enriquez, Lei Zhang, Yue Qi, Tim Karl, Nicola J. Lee, Felicia Reed |
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| Jazyk: | angličtina |
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Male Receptors Neuropeptide medicine.medical_specialty Science Regulator General Physics and Astronomy Neuropeptide FF receptor Adipose tissue Ligands General Biochemistry Genetics and Molecular Biology Article Bone and Bones 03 medical and health sciences Basal (phylogenetics) Adipose Tissue Brown Osteogenesis Internal medicine Brown adipose tissue medicine Animals Homeostasis Neuropeptide Y Neuropeptide FF RNA Messenger lcsh:Science Mice Knockout Neurons Multidisciplinary Behavior Animal Chemistry Neuropeptides Arcuate Nucleus of Hypothalamus Thermogenesis General Chemistry Diet Cold Temperature 030104 developmental biology Endocrinology medicine.anatomical_structure Female lcsh:Q Energy Metabolism Signal Transduction |
| Zdroj: | Nature Communications, Vol 9, Iss 1, Pp 1-19 (2018) Nature Communications |
| ISSN: | 2041-1723 |
| Popis: | 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. Excess caloric intake leads to increased thermogenesis in brown adipose tissue, to limit weight gain. Here, the authors show that neuropeptide FF receptor-2 signalling promotes thermogenesis via control of NPY expression in the arcuate nucleus, and that it absence in mice leads to a failure of activation of diet-induced thermogenesis and the development of exacerbated obesity. |
| Databáze: | OpenAIRE |
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