The role of nitric oxide signaling in food intake; insights from the inner mitochondrial membrane peptidase 2 mutant mice

Reactive oxygen species have been implicated in feeding control through involvement in brain lipid sensing, and regulating NPY/AgRP and pro-opiomelanocortin (POMC) neurons, although the underlying mechanisms are unclear. Nitric oxide is a signaling molecule in neurons and it stimulates feeding in ma...

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Bibliographic Details
Published in:Redox biology 2013-01, Vol.1 (1), p.498-507
Main Authors: Han, Changjie, Zhao, Qingguo, Lu, Baisong
Format: Article
Language:English
Subjects:
Adipose Tissue - drug effects
Animals
Body Weight - drug effects
Brain - cytology
Brain - drug effects
Cells, Cultured
Cyclic GMP - metabolism
Eating - drug effects
Eating - genetics
Endopeptidases - genetics
Energy expenditure
Female
Food intake
Gene Expression Regulation - drug effects
Immp2l
Male
Mice
Mitochondrial Proteins - genetics
Mutant mice
Mutation
Nitric oxide
Nitric Oxide - pharmacology
Reactive Oxygen Species - pharmacology
Research Paper
Signal Transduction - drug effects
Superoxide
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Summary:Reactive oxygen species have been implicated in feeding control through involvement in brain lipid sensing, and regulating NPY/AgRP and pro-opiomelanocortin (POMC) neurons, although the underlying mechanisms are unclear. Nitric oxide is a signaling molecule in neurons and it stimulates feeding in many species. Whether reactive oxygen species affect feeding through interaction with nitric oxide is unclear. We previously reported that Immp2l mutation in mice causes excessive mitochondrial superoxide generation, which causes infertility and early signs of aging. In our present study, reduced food intake in mutant mice resulted in significantly reduced body weight and fat composition while energy expenditure remained unchanged. Lysate from mutant brain showed a significant decrease in cGMP levels, suggesting insufficient nitric oxide signaling. Thus, our data suggests that reactive oxygen species may regulate food intake through modulating the bioavailability of nitric oxide.
ISSN:2213-2317
2213-2317
DOI:10.1016/j.redox.2013.10.003