Genotyping and Nucleotide Sequences of Growth Hormone Releasing Hormone and Its Receptor Genes in Egyptian Buffalo.

Aim: The hypothalamic hormone, growth hormone-releasing hormone, is the principal stimulator of pituitary growth hormone (GH) synthesis and secretion. GHRH and its receptor (GHRHR) provide important functions in the regulation of the GH axis and in the development and proliferation of pituitary somatotropic axis. This study aimed to identify the genotypes and nucleotide sequences of two multifunctional genes; growth hormone-releasing hormone (GHRH) and its receptor (GHRHR) in Egyptian buffalo. Methodology: Genomic DNA was extracted from blood samples of 100 healthy buffaloes maintained at the Mahlet Mussa and El-Gmeasa herds from 2010 to 2012. PCR was performed using primers flanking a 296-bp fragment from GHRH gene and a 425-bp fragment from GHRHR gene of Egyptian buffalo. The PCR-amplified fragments were digested with HaeIII (GHRH) and Eco57I (GHRHR), electrophoresed and analyzed on agarose gels stained with ethidium bromide. The two amplified fragments were also sequenced and aligned with published sequences. Results: Depending on the presence of the restriction site at 241

Growth hormone response to growth hormone-releasing peptide-2 in growth hormone-deficient Little mice

OBJECTIVE: To investigate a possible direct, growth hormone-releasing, hormone-independent action of a growth hormone secretagogue, GHRP-2, in pituitary somatotroph cells in the presence of inactive growth hormonereleasing hormone receptors. MATERIALS AND METHODS: The responses of serum growth hormone to acutely injected growth hormone-releasing P-2 in lit/litmice, which represent a model of GH deficiency arising frommutated growth hormone-releasing hormonereceptors, were compared to those observed in the heterozygous (lit/+) littermates and wild-type (+/+) C57BL/6J mice. RESULTS: After the administration of 10 mcg of growth hormone-releasing P-2 to lit/lit mice, a growth hormone release of 9.3±1.5 ng/ml was observed compared with 1.04±1.15 ng/ml in controls (p<0.001). In comparison, an intermediate growth hormone release of 34.5±9.7 ng/ml and a higher growth hormone release of 163±46 ng/ml were induced in the lit/+ mice and wild-type mice, respectively. Thus, GHRP-2 stimulated growth hormone in the lit/lit mice, and the release of growth hormone in vivo may be only partially dependent on growth hormone-releasing hormone. Additionally, the plasma leptin and ghrelin levels were evaluated in the lit/lit mice under basal and stimulated conditions. CONCLUSIONS: Here, we have demonstrated that lit/lit mice, which harbor a germline mutation in the Growth hormone-releasing hormone gene, maintain a limited but statistically significant growth hormone elevation after exogenous stimulation with GHRP-2. The present data probably reflect a direct, growth hormone-independent effect on Growth hormone S (ghrelin) stimulation in the remaining pituitary somatotrophs of little mice that is mediated by growth hormone S-R 1a.