| First Author | Mizuno TM | Year | 2013 |
| Journal | Behav Brain Res | Volume | 256 |
| Pages | 512-9 | PubMed ID | 24013028 |
| Mgi Jnum | J:207245 | Mgi Id | MGI:5554977 |
| Doi | 10.1016/j.bbr.2013.08.050 | Citation | Mizuno TM, et al. (2013) Mediation of glucose-induced anorexia by central nervous system interleukin 1 signaling. Behav Brain Res 256:512-9 |
| abstractText | Hypothalamic glucose sensing plays a critical role in the regulation of food intake and metabolism. Glucose injection, either centrally or peripherally suppresses food intake. However, the mechanism of glucose-induced feeding suppression is not fully understood. It has been demonstrated that hypothalamic interleukin 1 beta (IL-1beta) mRNA levels are altered by metabolic states and IL-1 signaling participates in the regulation of food intake. Therefore, we hypothesized that hypothalamic IL-1 gene expression is regulated by glucose and glucose-induced feeding suppression is mediated via hypothalamic IL-1 signaling. To address this hypothesis, we examined the effect of glucose on IL-1alpha and IL-1beta mRNA expression in the hypothalamus. We also examined the effect of intraperitoneal injection of glucose on food intake in wild-type and type I IL-1 receptor (IL-1RI)-deficient mice. Levels of IL-1alpha and IL-1beta mRNA in the hypothalamus were increased in response to feeding and intraperitoneal injection of glucose, and were positively correlated with blood glucose levels in mice. Exposure of hypothalamic explants to high glucose (10 mM) media increased IL-1alpha and IL-1beta mRNA levels compared to low glucose (1 mM) media. Intraperitoneal glucose administration reduced food intake in wild-type mice, while the feeding-suppressing effect of glucose was attenuated in IL-1RI-deficient mice. These findings support the role for hypothalamic IL-1 signaling in the mediation of the anorectic effect of glucose. |
