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  • In mammals a major physiological role

    2022-01-15

    In mammals, a major physiological role of the GHSR gene appears to be in regulating food intake and energy homeostasis by partaking in the neuronal mechanisms involving neuropeptide Y and agouti-related protein (Nakazato et al., 2001, Chen et al., 2017). In our study, determination of the abundance of GHSR1a mRNA in eight tissues showed that expression of GHSR1a was highest in the pituitary, an important part of the growth axis in mammals, indicating that GHSR1a is associated with growth traits in pigs. The GHRL (ghrelin)/GHSR/GH system plays a role in the control of a number of key pathways, including energy metabolism, GH secretion, and glucose metabolism (Lim et al., 2011, Abegg et al., 2017). Strikingly, the real-time PCR and western blotting assays showed that the GHSR1a expression levels in the pituitary and liver tissues of fast-growing Yorkshire pigs were higher than those in slow-growing breeds (Diannan small-eared and Tibetan pigs), indicating that GHSR1a might positively regulate the growth rate of pigs. This is consistent with a previous report, which showed that the GHSR1a expression levels were the highest in the pituitary and 745 receptor tissues in mice (Sun et al., 2007). The above findings provide evidence that an increased expression of GHSR1a is favorable to growth, showing that GHSR1a can promote animal growth. In conclusion, the genotype frequency distribution among pig breeds and the correlation analyses of genotype and growth rates using the SNP C-1595A of GHSR suggest that this SNP can influence growth traits and that the presence of the C-allele is advantageous for growth rate in pigs. An increase in the expression level of GHSR1a might facilitate an increase in the growth rate of pigs. Our study provides data that will be useful for molecular marker or functional gene analyses for improving the production performance of pigs. Further work will be necessary to confirm the potential of this SNP and to verify the function of the GHSR gene in economic traits in pigs.
    Introduction Ghrelin is a 28 amino acid peptide hormone secreted primarily from the X/A-like cells of the gastric oxyntic mucosa in the stomach [1], [2]. Ghrelin release is enhanced under conditions of negative energy balance and in anticipation of meals [3], [4], and ghrelin administration has the effect of increasing food intake and fat storage [5], [6]. In addition to its role in homeostatic feeding, ghrelin acts via the mesocorticolimbic dopamine system to mediate reward-seeking and motivated behaviors [7], [8], [9], [10]. Ghrelin is also released in response to psychosocial stress, where it may mediate the metabolic and behavioral adaptations that accompany the stress response [11], [12]. Ghrelin in circulation is found both in its native form and in the serine 3 acylated form commonly referred to as active ghrelin, since it is the only form capable of binding to the Growth Hormone Secretagogue Receptor 1a (GHSR1a), the only known receptor for ghrelin [13], [14]. The acyl-modification is uniquely catalyzed by Ghrelin O-acyl Transferase (GOAT), a member of the membrane-bound O-acyltransferase (MBOAT) family [13], [14], and mice lacking GOAT are entirely deficient in acylated forms of ghrelin [15]. The effects of ghrelin comprise not only consummatory behaviors, but also motivated and appetitive behaviors that often precede food intake. In humans there is an increase in circulating ghrelin in advance of meals [16], and a similar phenomenon occurs in rodents entrained to a scheduled mealtime [16], [17], [18], [19]. This increase in circulating ghrelin is correlated with an increase in locomotor activity [17], [20], [21]. This pattern of behavior, termed food anticipatory activity, is thought to reflect the foraging behaviors that an animal in the wild would normally exhibit under conditions of restricted food access [22]. Food anticipatory activity is enhanced by ghrelin administration in sated animals [23]. Moreover, food anticipatory activity is attenuated in mice lacking the ghrelin receptor (GHSR) [24], [23], as well as rats treated with ghrelin antagonists [21].