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Diet‐Induced Obesity Attenuates Fasting‐Induced Hyperphagia
Author(s) -
Briggs D. I.,
Lemus M. B.,
Kua E.,
Andrews Z. B.
Publication year - 2011
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/j.1365-2826.2011.02148.x
Subject(s) - orexigenic , endocrinology , medicine , arc (geometry) , ghrelin , neuropeptide y receptor , energy homeostasis , hypothalamus , appetite , neuropeptide , obesity , biology , chemistry , hormone , receptor , geometry , mathematics
Obesity impairs arcuate (ARC) neuropeptide Y (NPY)/agouti‐releated peptide (AgRP) neuronal function and renders these homeostatic neurones unresponsive to the orexigenic hormone ghrelin. In the present study, we investigated the effect of diet‐induced obesity (DIO) on feeding behaviour, ARC neuronal activation and mRNA expression following another orexigenic stimulus, an overnight fast. We show that 9 weeks of high‐fat feeding attenuates fasting‐induced hyperphagia by suppressing ARC neuronal activation and hypothalamic NPY/AgRP mRNA expression. Thus, the lack of appropriate feeding responses in DIO mice to a fast is caused by failure ARC neurones to recognise and/or respond to orexigenic cues. We propose that fasting‐induced hyperphagia is regulated not by homeostatic control of appetite in DIO mice, but rather by changes in the reward circuitry.