| First Author | Lob HE | Year | 2017 |
| Journal | JCI Insight | Volume | 2 |
| Issue | 2 | Pages | e87094 |
| PubMed ID | 28138551 | Mgi Jnum | J:290644 |
| Mgi Id | MGI:6443255 | Doi | 10.1172/jci.insight.87094 |
| Citation | Lob HE, et al. (2017) Deletion of p22(phox)-dependent oxidative stress in the hypothalamus protects against obesity by modulating beta3-adrenergic mechanisms. JCI Insight 2(2):e87094 |
| abstractText | A role for oxidative stress in the brain has been suggested in the pathogenesis of diet-induced obesity (DIO), although the underlying neural regions and mechanisms remain incompletely defined. We tested the hypothesis that NADPH oxidase-dependent oxidative stress in the paraventricular nucleus (PVN), a hypothalamic energy homeostasis center, contributes to the development of DIO. Cre/LoxP technology was coupled with selective PVN adenoviral microinjection to ablate p22(phox) , the obligatory subunit for NADPH oxidase activity, in mice harboring a conditional p22(phox) allele. Selective deletion of p22(phox) in the PVN protected mice from high-fat DIO independent of changes in food intake or locomotor activity. This was accompanied by beta3-adrenoceptor-dependent increases in energy expenditure, elevations in brown adipose tissue thermogenesis, and browning of white adipose tissue. These data reveal a potentially novel role for brain oxidative stress in the development of DIO by modulating beta3-adrenoceptor mechanisms and point to the PVN as an underlying neural site. |
