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Mol Metab. 2014 May 14;3(5):581-91. doi: 10.1016/j.molmet.2014.05.001. eCollection 2014 Aug.

Stress- and diet-induced fat gain is controlled by NPY in catecholaminergic neurons.

Author information

1
Neuroscience Division, Garvan Institute of Medical Research, St Vincent's Hospital, Sydney 2010, Australia ; St Vincent's Clinical School, UNSW Australia, Sydney 2052, Australia.
2
Neuroscience Division, Garvan Institute of Medical Research, St Vincent's Hospital, Sydney 2010, Australia.
3
Osteoporosis and Bone Biology Division, Garvan Institute of Medical Research, St Vincent's Hospital, Sydney 2010, Australia.
4
Department of Pharmacology, Drug Development and Therapeutics, University of Turku, Finland.
5
Neuroscience Division, Garvan Institute of Medical Research, St Vincent's Hospital, Sydney 2010, Australia ; Faculty of Medicine, UNSW Australia, Sydney 2052, Australia.

Abstract

Neuropeptide Y (NPY) and noradrenaline are commonly co-expressed in sympathetic neurons. Both are key regulators of energy homeostasis and critical for stress-coping. However, little is known about the specific function of NPY in the catecholaminergic system in these regulations. Here we show that mice with NPY expression only in the noradrenergic and adrenergic cells of the catecholaminergic system (catNPY) exhibited exacerbated diet-induced obesity, lower body and brown adipose tissue temperatures compared to WT and NPY(-/-) mice under a HFD. Furthermore, chronic stress increased adiposity and serum corticosterone level in WT but not NPY(-/-) mice. Re-introducing NPY specifically to the catecholaminergic system in catNPY mice restored stress responsiveness associated with increased respiratory exchange ratio and decreased liver pACC to tACC ratio. These results demonstrate catecholaminergic NPY signalling is critical in mediating diet- and chronic stress-induced fat gain via effects on diet-induced thermogenesis and stress-induced increases in corticosterone levels and lipogenic capacity.

KEYWORDS:

Adiposity; Catecholaminergic neurons; Energy homeostasis; Neuropeptide Y; Stress

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