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    • In this study we saw change in GHS

    2021-11-30

    In this study, we saw change in GHS-R1a mRNA expression in fasting condition. It is noteworthy that changes in ghrelin and GHS-R1a mRNA expression synchronized in organs were examined. In the BAF312 and pituitary, gene expression increased 4days after fasting, and the increased level declined until 2weeks after fasting. There are a few reports about expression changes in brain GHS-R1a mRNA in other animals, and period of sampling seems to affect the results. In rats, GHS-R1a mRNA expression in the arcuate nuclei of the hypothalamus increases 48h after fasting (Nogueiras et al., 2004). Peddu et al. (2009) have reported a high expression level of GHSR1a-LR mRNA in whole brain of tilapia 3h before meal. On the contrary, in a long-term experiment, receptor density does not change by nutritional state in the rat hypothalamus (Harrold et al., 2008). In tilapia, brain expression of GHSR1a-LR mRNA did not change for 7days of fasting (Riley et al., 2008). GHS-R1a mRNA expression did not change in the brain of bullfrog for 20days of fasting (Kaiya et al., 2011a). These results indicate that GHS-R1a mRNA expression in the central nervous system responds at relatively early time after it was gone without food. In newts, gastric expressions of ghrelin and GHS-R1a mRNA transiently decreased 4days after fasting, and significantly increased 2weeks after fasting. This pattern of change is different from that of the brain or pituitary. We observed a similar result in frogs: expression of ghrelin and GHS-R1a mRNA in the stomach increased 10days after food deprivation (Kaiya et al., 2006, Kaiya et al., 2011a). Expression of gastric GHS-R1a mRNA may synchronize with ghrelin mRNA expression for binding ghrelin just after releasing from the stomach. The reason that expression response in the stomach is slower when compared to that in brain is not clear, but it may be because amphibian can relatively endure starvation (low energy balance). In summary, we determined cDNA sequence of functional ghrelin receptor (GHS-R1a) in Japanese fire belly newt. The newt GHS-R1a showed apparent ligand selectivity between Ser3-ghrelin and Thr3-ghrelin. The GHS-R1a mRNA was detected in various organs including the brain and intestinal tract, suggesting ghrelin's physiological effects. Fasting affected GHS-R1a mRNA expression, and up-regulated with different time course in the central nervous system including the brain, pituitary and peripheral stomach, suggesting that ghrelin is involved in energy homeostasis in the newt at least.
    Acknowledgments We thank Mrs. Azumi Ooyama for excellent technical assistance. This work was supported in part by JSPS KAKENHI grant numbers 23570086, 26440174 to HKai.
    Cognitive control of feeding Feeding behavior is controlled by direct and indirect mechanisms. Direct control is achieved through release of gastrointestinal (GI) peptides as nutrients accumulate during a meal. The net result of this meal-induced feedback is stimulation of satiety mechanisms that reduce food intake. It is important to point out here that the hindbrain is a critical region that integrates ascending signals from the GI tract and descending input from the central nervous system (CNS) to limit feeding behavior (Begg and Woods, 2013, Bray, 2000, Coll et al., 2007, Cummings and Overduin, 2007, Moran, 2004, Schwartz et al., 2000). In contrast indirect control of feeding behavior occurs through activation of forebrain and hypothalamic regions that stimulate meal anticipation and meal initiation. Importantly, indirect controls can override hindbrain satiety mechanisms to allow feeding to continue once energy reserves have been met. Moreover, indirect controls of feeding can be initiated by cues in the environment (Balleine, 2005, Holland and Petrovich, 2005, Johnson, 2013, Petrovich, 2011, Petrovich et al., 2005, Sobik et al., 2005, Yu et al., 2015) or those that inform an individual about metabolic state (Davidson et al., 2009, Davidson and Jarrard, 1993). The ability to anticipate a meal occurs secondary to mnemonic processes that enable environmental cues linked to receipt of food to acquire salience. In turn, these environmental cues stimulate anticipation of scheduled meals; thereby enabling increases in meal size, and increased body weight gain (Woods, 1991). When persistent, these indirect controls produce maladaptive changes in the CNS that diminish the homoeostatic control of food intake and produce excess body weight gain (Gearhardt et al., 2012, Gormally et al., 1982). Understanding the sequence of events that allow indirect controls to stimulate feeding in the absence of caloric need will provide better strategies to combat obesity. Presently, we know that cognitive control of feeding behavior involves communication between forebrain and hypothalamic brain regions to stimulate food anticipation and food intake.