| First Author | Kong D | Year | 2010 |
| Journal | Cell Metab | Volume | 12 |
| Issue | 5 | Pages | 545-52 |
| PubMed ID | 21035764 | Mgi Jnum | J:167906 |
| Mgi Id | MGI:4881350 | Doi | 10.1016/j.cmet.2010.09.013 |
| Citation | Kong D, et al. (2010) Glucose stimulation of hypothalamic MCH neurons involves K(ATP) channels, is modulated by UCP2, and regulates peripheral glucose homeostasis. Cell Metab 12(5):545-52 |
| abstractText | Blood glucose levels are tightly controlled, a process thought to be orchestrated primarily by peripheral mechanisms (insulin secretion by beta cells, and insulin action on muscle, fat, and liver). The brain also plays an important, albeit less well-defined role. Subsets of neurons in the brain are excited by glucose; in many cases this involves ATP-mediated closure of K(ATP) channels. To understand the relevance of this, we are manipulating glucose sensing within glucose-excited neurons. In the present study, we demonstrate that glucose excitation of MCH-expressing neurons in the lateral hypothalamus is mediated by K(ATP) channels and is negatively regulated by UCP2 (a mitochondrial protein that reduces ATP production), and that glucose sensing by MCH neurons plays an important role in regulating glucose homeostasis. Combined, the glucose-excited neurons are likely to play key, previously unexpected roles in regulating blood glucose. |
