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.
Keywords: ADSC, adipose-derived stromal cells; AMPK, AMP-activated protein kinase.; AgRP, agouti related protein; CART, cocaine- and amphetamine-regulated transcript; CYC1, cytochrome c1; Energy expenditure; Food intake; GPD2, mitochondrial glycerol phosphate dehydrogenase; Immp2l; Immp2l, IMP2 inner mitochondrial membrane peptidase-like; Mutant mice; NO, nitric oxide; NOS, nitric oxide synthase; NPY, neuropeptide Y; Nitric oxide; POMC, pro-opiomelanocortin; ROS, reactive oxygen species; Superoxide; UCP2, uncoupling protein 2; cGMP, cyclic guanosine monophosphate.