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. Author manuscript; available in PMC: 2014 Jul 2.
Published in final edited form as: Obes Rev. 2011 Apr;12(4):261–271. doi: 10.1111/j.1467-789X.2010.00770.x

Figure 1.

Figure 1

Potential pathways by which nesfatin-1 induces a sustained and prolonged reduction of dark phase food intake and delays gastric emptying in rats as suggested by pharmacological interventions and neuroanatomical approaches. Central nesfatin-1/NUCB2 mediates its anorexigenic effect via activation of melanocortin3/4 and CRF2 signalling and also by hyperpolarizing neurons containing the orexigenic peptide, neuropeptide Y. Nesfatin-1 also activates the hypothalamic magnocellular oxytocinergic system which could reduce food intake and delay gastric emptying. Peripheral nesfatin-1 can reach the brain via the circulation and crossing the blood-brain barrier and/or direct action on circumventricular organs as well as modulation of vagal afferent activity. +, stimulation; −, inhibition; ↓, reduction; Arc, arcuate nucleus; NPY, neuropeptide Y; NTS, nucleus of the solitary tract; PVN, paraventricular nucleus of the hypothalamus; SON, supraoptic nucleus (7,15,22,23,25).