AgRP ELISA Kit

Despite vast research attention, the knowledge about central mechanisms of appetite regulation in teleost remains inconclusive. A common strategy in studies on appetite regulating mechanisms is to measure the response to feed restriction or - deprivation, but responses vary between fish species and between experiments, and are also likely dependent on the degree of energy perturbation. The anadromous Arctic charr is an interesting model for studying appetite regulation as its feeding cycle comprises months of winter anorexia, and hyperphagia during summer. Here we studied how the gene expression of putative hypothalamic appetite regulators were affected by two days, one week and one month feed deprivation during summer, and subsequent re-feeding and exposure to feed flavour. Short-term feed deprivation caused only a minor reduction in condition factor and had no effect on hypothalamic gene expression. Long-term feed-deprivation caused a marked reduction in weight and condition factor which contrasted the increase in weight and condition factor seen in ad libitum fed controls. A marked energy perturbation by feed deprivation was also indicated by a lower hypothalamic expression of the genes encoding insulin-like growth factor 1 (IGF1) and IGF1 binding protein 5 in the feed deprived charr compared to fed controls. Surprisingly, long-term feed deprivation and energy perturbation did not induce changes in hypothalamic appetite regulators. Unexpectedly, re-feeding and exposure to feed flavour caused an increase in the expression of the genes encoding the orexigenic agouti-related peptide and the anorexigenic melanocortin receptor 4 and cocaine- and amphetamine-regulated transcript. Our study gives strong evidence for a role of these in appetite regulation in Arctic charr, but their mechanisms of action remain unknown. We suggest that changes in gene expression are more likely to be registered during transition phases, e.g. from fasting to feeding and upon stimulatory inputs such as feed flavour. (C) 2017 Elsevier Inc. All rights reserved.

Binge eating disorder (BED) is an eating disorder involving repeated, intermittent over consumption of food in brief periods of time, usually with no compensatory behaviors. There are few successful treatments and the underlying neural mechanisms remain unclear. In the current study, we hypothesized that voluntary running wheel (RW) activity could reduce binge-like eating behavior in a rat model. Rats were given intermittent (3 times/wk) limited (1hr) access to a high-fat food (Crisco), in addition to continuously available chow. Crisco was available every Mon, Wed, and Fri for 1hr before dark onset. Rats were divided into 2 groups: those with RW access during the first half of the experiment and sedentary during the second half (RW-SED) and those that were sedentary during the first half of the experiment and had RW access during the second half (SED-RW). Crisco intake was significantly less in both groups during the period of time with a RW present. Within the bingeing RW-SED rats, the gene expression of the orexigenic neuropeptides AgRP and NPY were similar to a non-bingeing sedentary control (CON) group, while the expression of the anorexigenic neuropeptide POMC was significantly increased relative to the SED-RW and CON groups. Despite elevated POMC, the rats continued to binge. Additionally, within both groups, the gene expression of the D2R and Oprm1 in the NAc and the VTA were altered suggesting that the reward system was stimulated by both the bingeing behavior and the running wheel activity. Overall, access to a RW and the resulting activity significantly reduced binge-like behavior as well as modulated the effects of binging on brain appetite and reward systems.