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  • In terms of stimulation oxytocin dopamine noradrenaline adre


    In terms of stimulation, oxytocin, dopamine, noradrenaline, adrenaline and glucagon have all been reported to increase ghrelin secretion (Mundinger et al., 2006, Iwakura et al., 2011, de la Cour et al., 2007, Gagnon and Anini, 2013). Stimulatory effects on ghrelin secretion have also been observed with cannabinoids. Specifically pharmacological administration of the endogenous cannabinoid anandamide and CPP-540, a synthetic cannabinoid receptor-1 (CB1R) agonist, stimulate ghrelin secretion. In addition these two compounds reduced X/A cell ghrelin immunoreactivity indicating that CB1R activation promotes GI ghrelin secretion (Zbucki et al., 2008). More recent work on this topic indicates that the CB1R stimulatory affects on ghrelin secretion likely involve cannabinoid-induced activation of the mTOR pathway (Senin et al., 2013).
    Summary To summarize, hunger and appetite are controlled by a distributed set of CNS nuclei that collectively regulate a variety of processes that promote food intake including: consolidation of environmental cues that signal availability of food, motivate behavior to obtain food, initiate feeding behavior and increase meal size. Ghrelin is a GI peptide that informs and in some cases controls these processes Fig. 1. Thus understanding the central and peripheral controllers of GI ghrelin secretion, how these processes adapt across time, environment and metabolic status, can yield new treatment strategies for feeding pathologies and obesity.
    Acknowledgement This work was supported in part by funds provided for medical and biological research by the State of Washington Initiative Measure No. 171, administered by the WSU Alcohol and Drug Abuse Research Program.
    Overview of the Ghrelin Receptor
    The Ghrelin Receptor and Energy Metabolism Energy homeostasis is determined by the balance between alisertib intake (food ingestion) and energy expenditure (activity and/or heat production); even a slight imbalance over prolonged periods can lead to changes in body composition and result in the development of obesity, insulin resistance and other serious metabolic disorders. Ghrelin functions as a key modulator of energy homeostasis, acting via the ghrelin receptor to regulate appetite, select fuel substrate, modulate body weight, and maintain glucose/lipid homeostasis. Ghrelin may also signal the peripheral energy supply status to the brain through the ghrelin receptor, leading to changes in food intake and adiposity.113, 114 Ghrelin and its receptor therefore play an important role in enabling adaptation to changes in nutritional status by controlling metabolic parameters such as energy intake and expenditure.
    Strategies for Treatment of Obesity and Diabetes Ghrelin has been emerging as an attractive target for treatment of obesity and diabetes because of its profound effects on food intake and energy metabolism and its unique posttranslational modification by ghrelin O-acyl transferase (GOAT), which was identified as a conserved orphan membrane-bound enzyme by two different research groups in 2008.152, 153 Several reviews have already offered detail discussions on this issue. Here, we focus our discussion on the current challenges facing therapeutic strategies for obesity and diabetes.
    Introduction Des-acyl ghrelin (DAG), together with ghrelin and obestatin, form the products of the prepro-ghrelin gene (Chen et al., 2009). Ghrelin has been given the most attention since its discovery, with DAG being initially regarded as a non-functional ghrelin ligand. This stance towards DAG has changed in the recent years after identifying various physiological processes regulated by this peptide (Baldanzi et al, 2002, Bedendi et al, 2003, Lear et al, 2010, Muccioli et al, 2004). Both ghrelin and DAG share an identical amino acid sequence, with the only difference that DAG lacks an O-n-octanoylation at serine 3 (Chen et al., 2009). This was believed to render DAG unable to bind with the growth hormone secretagogue receptor (now preferably denoted as ghrelin receptor (IUPHAR/BPS, 2015), and numerous studies have been performed to try to elucidate the receptor on which DAG exerts its function (Bulgarelli et al, 2009, Delhanty et al, 2012, Delhanty et al, 2013, Pei et al, 2014).