Selection based on molecular markers is one of the new methods that may improve progress and accuracy of selection in animal breeding programs. The GHRH gene (Growth hormone-releasing hormone) is a candidate gene for marker-assisted selection strategies. Polymorphs of GHRH gene are reported to be significantly associated with milk production and constituent traits. In order to study the polymorphism of GHRH gene, blood samples were collected from 112 Sarabi cows. Genomic DNA was extracted and a fragment of 297 bp in size was amplified using polymerase chain reaction. The amplified fragments were subjected to restriction digestion with HaeIII endonuclease enzyme and the resultant digested products were run on 2% Agarose gel. The results revealed the existence of two alleles of GHRHA and GHRHB for the examined locus with frequencies of 0.19 and 0.81 respectively. Three different genotypic variants including GHRHA GHRHA, GHRHA GHRHB and GHRHB GHRHB were identified with genotypic frequencies of 0.0357, 0.3037 and 0.6607 respectively. The  c2 test showed that population is in Hardy-Weinberg equilibrium (P<0.05). These data provide evidence that sarabi cattle breed have a genetic variability, which opens interesting prospects for future selection programs, especially marker-assistant selection.

Growth hormone (GH) is a single polypeptide hormone which is produced and secreted by cells of the anterior pituitary gland. This hormone exerts diverse Growth promoting and metabolic effects. As GH circulates in the blood, it binds to GH receptors (GHR), a trans membrane protein expressed on the surface of liver, adipose, kidney, heart, intestine, lung and muscle cells. After receptor binding, GH induces GHR dimerization and JAK2 is activated after its association with a dimerized GHR. A Growth hormone antagonist (GHA) was produced in E.coli by a mutation that would block GH by preventing the GHR dimerization. In this study, we evaluated the effect of mutagenesis on binding energy of GH and GHA to their related receptor. The Growth hormone and its mutant 3D structures were obtained from PDB (http://www.rcsb.org/pdb/home) and M4T server, respectively. Likewise, GHR conformational structure, was found in NCBI (http://www.ncbi.nlm.nih.gov). GH and GHA affinity for binding to GHR was analyzed by HEX docking software and energy total (E total) was obtained. GH and GHA E total were -648.13 and -698.68 respectively. This data demonstrates that GHA affinity for binding to GHR is higher than GH affinity. So GHA in completion to GH will overcome GH in binding to GHR, it can act as an antagonist to prevent excessive Growth and cure acromegaly, diabetes and cancer.

The aim of this study is to evaluate the influence of Growth hormone on some interleukins levels in patients with Growth hormone deficiency by measuring and correlating many biochemical markers. Blood samples were gathered from study participants to estimate levels of basal Growth hormone, Growth hormone after 60 min (GH2) and 90 min (GH3) induction with clonidine, respectively, Insulin-like Growth factor, interleukin-4, interleukin-6, and resistin. The outcomes of the anthropometric measurements of the studied groups exposed a significant (p < 0,05) differences in mean of BMI and BMI Z score between the GHD and non-GHD. The outcomes presented significant (P < 0.05) decrease in levels of basal GH, GH2, GH3, and IGF-1 in the GHD compared to the non-GHD. The outcomes presented a significant (p<0.05) fall in level of IL-4, IL-6 and resistin in the GHD compared to the non-GHD. The breakdown of the study groups revealed that males made up (53.3%) of the GHD, while females made up (46.7%), whereas the non-GHD (64.4% males and 35.6% females). The percentage of underweight in the GHD (71.1%) was lower than in the non-GHD (80%), whereas the percentage of normal weight was greater in the non-Growth hormone deficiency (20%) compared to the GHD (17.8%). The distribution of the studied groups by gender displayed that non-significant (p>0.05) variances were seen in basal GH level, GH2, GH3 between males and females, IGF-1 was significant (p<0.05) decreases in males compared with females.

There are numerous, often contradictory reports on the effect of Growth hormone (GH) therapy on thyroid function. These reports prompted us to evaluate the impact of GH therapy on thyroid function in previously euthyroid children with GH deficiency. Twenty five clinically and biochemically euthyroid children with GH deficiency were studied. A thyroid profile (T4, Free T4, T3 and TSH) was performed at baseline and 3, 6 and 12 months after GH therapy in 21 children with idiopathic Growth hormone deficiency (group A) and 4 children with organic GH deficiency (group B). We observed a significant reduction in serum T4 and free T4 concentrations during GH therapy in both groups (P<0.01). No patient in group A had free T4 levels fell into the hypothyroid range, while in one of four patients in group B, free T4 value fell into the hypothyroid range during GH therapy. In both groups, no significant variation in serum TSH and T3 was recorded at any time. Our data suggest that GH therapy can introduce changes in thyroid function and so confirm the need of a careful monitoring of thyroid function in particular in children with organic GH deficiency during long-term GH therapy.

Background: Growth hormone (GH) produced by the somatotropic cells on the anterior part of the hypophysis.Its clinical application for many years was restricted to GH deficient children, but in recent years it has been widened to various other clinical conditions, not necessarily related to short stature. Currently, FDA has approved its usage in children with GH deficiency, Turner or Noonan syndromes, chronic renal failure, children born small for gestational age (SGA) and Prader-Willi syndrome. The aim of this paper was to summarize the current data on GH administration in modern pharmacotherapy.