Neuropeptides RSS feed: Articles in Press. The aim of Neuropeptides is the rapid publication of original research and review articles, dealing with the structure, distribution, actions and functions of peptides in the central and peripheral nervous systems. The explosion of research activity in this field has led to the identification of numerous naturally occurring endogenous peptides which act as neurotransmitters, neuromodulators, or trophic factors, to mediate nervous system functions. Increasing numbers of non-peptide ligands of neuropeptide receptors have been developed, which act as agonists or antagonists in peptidergic systems. The journal provides a unique opportunity of integrating the many disciplines involved in all neuropeptide research. The journal publishes articles on all aspects of the neuropeptide field, with particular emphasis on gene regulation of peptide expression, peptide receptor subtypes, transgenic and knockout mice with mutations in genes for neuropeptides and peptide receptors, neuroanatomy, physiology, behaviour, neurotrophic factors, preclinical drug evaluation, clinical studies, and clinical trials. Original papers predominate. Manuscripts may be of any length, but must be complete studies; preliminary communications are not accepted. Review articles and hypothesis papers are welcomed, and will be evaluated in the same way as experimental papers. Authors intending to submit a review are advised to communicate their intentions to the Editor, to avoid possible duplication. To order this journal online, visit http://intl.elsevierhealth.com/journals/npep http://www.neuropeptidesjournal.com//inpress?rss=yesElsevier Inc.en © 2012 Elsevier Ltd. All rights reserved. Neuropeptides0143-41792012-05-10 © 2012 Elsevier Ltd. All rights reserved. healthpermissions@elsevier.comhttp://www.neuropeptidesjournal.com/article/PIIS014341791200039X/abstract?rss=yesAbstract: Peptide YY (PYY) is best known for its important role in appetite regulation, but recent pharmacological studies have suggested that PYY is also involved in regulating energy balance and glucose homeostasis. However, the mechanism behind the regulation of these parameters by PYY is less clear. Here, by utilising an inducible transgenic mouse model where PYY overexpression is induced in adult animals (PYYtg) and release of mature PYY peptides is controlled by endogenous machineries, we show that elevating PYY levels leads to reduced food intake after a 24-h fast. Furthermore, PYYtg mice, although not significantly different from WT with respect to body weight, adiposity, lean mass, physical activity or energy expenditure, exhibited a significantly increased respiratory exchange ratio (RER), indicating decreased lipid oxidation and/or increased lipogenesis. Importantly, PYYtg mice showed a 25% reduction in liver protein levels of phosphorylated acetyl-CoA carboxylase (pACC) in the absence of changes in total ACC levels compared to those of WT mice. Moreover, liver protein levels of AMP-activated kinase (AMPK) in PYYtg mice were 25% lower than those of WT mice, consistent with a reduced pACC in these mice. These data suggest that elevation of PYY levels as seen after a meal can increase lipogenic capacity, which is likely a key contributor to the increased RER seen in PYYtg mice. In addition, PYYtg mice exhibited comparable insulin tolerance and oral glucose tolerance to those of WT, but showed a trend towards decreased insulin levels in response to an oral glucose challenge, indicating that PYY could improve insulin action. Taken together, these findings demonstrate that under physiological conditions, PYY reduces food intake while enhancing lipogenic capacity and insulin action, likely contributing to fuel assimilation in the postprandial state.Adult-onset PYY overexpression in mice reduces food intake and increases lipogenic capacity - Corrected ProofYan-Chuan Shi, Constanze Hämmerle, I-Chieh Jennifer Lee, Nigel Turner, Amy D. Nguyen, Sabrina J. Riepler, Shu Lin, Amanda Sainsbury, Herbert Herzog, Lei Zhang10.1016/j.npep.2012.04.001Neuropeptides (2012)2012-05-10Neuropeptides2012-05-10