To be or NUCB2, is nesfatin the answer? Michael A. Cowley, Kevin L. Grove  Cell Metabolism  Volume 4, Issue 6, Pages 421-422 (December 2006) DOI: 10.1016/j.cmet.2006.11.001 Copyright © 2006 Elsevier Inc. Terms and Conditions

Figure 1 Schematic of possible NUCB2 neuronal pathways NUCB2 expressing neurons (green) are found in several regions of the brain. Some neurons in the parvocellular PVH (pPVH) express NUCB2 and the melanocortin receptor (MC4) and receive input from α-MSH and AgRP fibers. α-MSH increases the expression and release of nesfatin-1. Oh-I and colleagues (2006) propose that NUCB2 neurons in the pPVH cause anorexia by secretion of nesfatin-1, although the site of action of nesfatin-1 remains unknown. Fasting causes changes in levels of peripheral metabolic signals (i.e., leptin and ghrelin), which act through the arcuate nucleus (ARH) to decrease the activity of POMC neurons (dark blue) and increase the activity of AgRP neurons (light blue). Oh-I and colleagues propose that fasting decreases activity of pPVH NUCB2 neurons via a melanocortin dependent pathway. Several other pathways also deserve consideration. Stress also causes anorexia, and it may do so by activating NUCB2 neurons in the pPVH. Magnocellular neurons in the supraoptic nucleus (SON) and PVH (mPVH) are known to project to the posterior pituitary and regulate fluid balance. NUCB2 neurons in these regions may indirectly affect food intake by changing fluid balance. Surprisingly, NUCB2 neurons in the mPVH, SON, ARH, lateral hypothalamus/zona incerta (LHA/ZI), and nucleus of the solitary tract (NTS) were not affected by fasting or melanocortins, and thus their functions remain unclear. Cell Metabolism 2006 4, 421-422DOI: (10.1016/j.cmet.2006.11.001) Copyright © 2006 Elsevier Inc. Terms and Conditions