Disease relevance of GHRH

• In Exp. 2, intracerebroventricular (icv) and intravenous (iv) injections of MEL (100 mug) and GH-releasing hormone (GHRH; 0.25 mug/kg body weight), respectively, were performed simultaneously to examine the effect of MEL on GHRH-induced GH release [1].
• Use of the HIV-1 protease for excision of growth-hormone-releasing factor from synthetic and recombinant peptide precursors [2].
• Development of a recombinant bovine leukemia virus vector for delivery of a synthetic bovine growth hormone-releasing factor gene into bovine cells [3].
• Modification of the carboxy-terminal amino acid sequence alters the Escherichia coli expression of a gene encoding multiple repeats of a bovine growth hormone releasing factor analog [4].
• Average daily gain and days on feed were not affected by treatments, but TRF treatment increased (P less than .05) total intake of dry matter (DM) and feed conversion ratio: 3.00, 3.02, 3.08, and 3.22 kg DM/kg weight gain for control, GRF, TRF, and GTRF, respectively [5].

Psychiatry related information on GHRH

• Similarly, neither growth hormone-releasing factor nor growth hormone altered the mRNA abundance of the erythrocyte-type or the intestinal-type glucose transporter in the kidney, but large individual differences were observed in the mRNA abundance of the intestinal-type glucose transporter in liver [6].

High impact information on GHRH

• RESULTS: In the study case, circulating autoantibodies selectively decorated median eminence dopaminergic nerve terminals, as well as pituitary gonadotropes, but not GHRH nerve terminals or pituitary somatotropes [7].
• At 18 days after plasmid administration, GHRH-treated animals had increased numbers of CD2(+) alphabeta T-cells (P < 0.004), CD25(+)CD4(+) cells (P < 0.0007), and CD4(+)CD45R(+) cells (P < 0.016) compared to controls [8].
• At 300 days post-GHRH therapy, CD45R(+)/CD45R0(-) naïve lymphocytes were significantly increased in frequency (P < 0.05) [8].
• The 5' flanking sequences of the two GRF genes were compared and regions of homology and divergence identified [9].
• The mRNAs of the GRF genes are encoded by six exons interrupted by five introns [9].

Chemical compound and disease context of GHRH

• After a 5-wk growth period, all steers were challenged (intravenous injection) over a 3-wk period with three levels of a combination of TRH + GHRH (0.1 + 0.01, 1.0 + 0.1, 2.5 + 0.25 microg/kg body weight, respectively) [10].

Biological context of GHRH

• No adverse effects were associated with either the plasmid delivery or GHRH expression [8].
• 8. Both basal and GHRH-stimulated GH secretion were unaffected by TTX, implying that the Na+ action potential is not critical for such release [11].
• The venous injection of either GHRH (0.25 microg/kg) or GHRP-6 (2.5 microg/kg) significantly increased plasma GH concentrations in both 3- and 12-week-old animals, but GH AUC was significantly greater in 3-week-old than in 12-week-old animals [12].
• The 5 cows in group A received GHRH analog during period 1 (from d 22 to 42 postpartum) and saline during period 2 (from d 57 to 77 postpartum), and those in group B received saline and GHRH analog during periods 1 and 2, respectively [13].
• Growth hormone response to GHRH is modestly related to body composition but not to ADG in weanling beef heifers and likely has limited use in evaluation of growth performance in replacement beef heifers [14].

Anatomical context of GHRH

• The [Ca2+]i oscillations seen in a proportion of the somatotrophs were modulated in frequency by GHRH and SS, and are probably generated by influx of Ca2+ through channels in the cell membrane [15].
• We conclude that GHRP-6 acts at the hypothalamus to stimulate secretion of GHRH, and at somatotropes to restore and enhance the responsiveness of somatotropes to GHRH [16].
• To test the hypothesis that leptin directly affects basal and GHRH-mediated GH secretion from the adenohypophysis, we examined the effects of various doses of recombinant ovine leptin (oleptin) on perifused adenohypophyseal (AP) explants and compared responses of tIssues from control and fasted cows [17].
• Clonidine failed to alter release of GHRH or SRIH from hypothalamic slices, but stimulated release of GHRH from explants of hypophysial stalk [18].
• Our first objective was to determine if stimulation of alpha(2)-adrenergic receptors increases activity of GHRH neurons in the arcuate nucleus (ARC) and/or decreases activity of SRIH neurons in periventricular (PeVN) and ARC nuclei [18].

Associations of GHRH with chemical compounds

• Similar results were obtained with GHRH, 10(-9) M, with or without atropine, 10(-7) M [19].
• The special characteristic of all four GHRH analogs is that arginine was replaced by agmatine (Agm) in Position 29 [20].
• After an additional 3 wk, steers were reimplanted and a second 5-wk growth period was followed by a single challenge of the 1.0 + 0.1 TRH + GHRH dose level [10].
• Similar results, including significant stimulation of splenocyte responses to ConA, LPS, and PHA, were obtained in MT-hGHRH transgenic mice in which overexpression of GHRH leads to striking pituitary enlargement and massive elevation of peripheral levels of homologous (mouse) GH [21].
• Blockade of SRIH receptors enabled clonidine to stimulate release of GHRH from slices of hypothalami, but also stimulated release of SRIH [18].

Regulatory relationships of GHRH

• Therefore, we wanted to determine if GHRP-6 stimulated secretion of GHRH or inhibited secretion of somatostatin, or both [16].

Other interactions of GHRH

• Predicting growth in angus bulls: the use of GHRH challenge, insulin-like growth factor-I, and insulin-like growth factor binding proteins [22].
• The K+ channel blocker TEA stimulated GH release above basal and GHRH-stimulated levels [11].
• Clones and controls were challenged with GH-releasing hormone (GHRH) (3 microg/100 kg body weight) and somatostatin (somatotropin release-inhibiting factor [SRIF]) (1.87 and 5 microg/100 kg body weight) at 14 mo of age [23].
• The interactive effects of VIP, PHI, GHRH, and SRIF on the release of growth hormone from cultured adenohypophysial cells in cattle [24].
• The objective of this study was to evaluate the effects of recombinant bovine growth hormone-releasing factor (rGRF) or recombinant bovine somatotropin (rbST) on growth and function of the first-wave dominant follicle and corpus luteum [25].

Analytical, diagnostic and therapeutic context of GHRH

• Intravenous injection of GHRH dramatically increased GH release [1].
• The growth hormone releasing factor was structurally characterized by gas phase sequence analysis [26].
• In the third trimester of pregnancy, 32 heifers received 2.5 mg of a myogenic GHRH-expressing plasmid by intramuscular injection followed by electroporation, while 20 heifers were used as controls [8].
• Dual-label immunohistochemistry was performed on free-floating sections of hypothalami using antibodies directed against Fos and Fos-related antigens (Fos/FRA) as a marker of neuronal activity in immunoreactive GHRH and SS neurons [27].
• Coronal and sagittal frozen sections (30-60 microns) of Zamboni's fixed hypothalamic tissue, without prior colchicine treatment were incubated with GHRH or SS primary antisera for 48 h, then visualized by peroxidase-diaminobenzidine immunocytochemistry [28].

References