Effect of recombinant growth hormone [rh-GH] on glycerol induced acute renal failure [ARF] in rats

Experimental studies showed that acute uremia is characterized by reduced GH and IGF-l messenger RNA expression and is manifested as resistance to human rh-GH. However the administration of high doses of several anabolic agents including rh-GH have been proposed as a potential therapy for several catabolic conditions including acute renal failure [ARF]. Therefore this study was conducted to reveal the renoprotective and ameliorating effects of GH on glycerol-induced ARF in rats, by exploring its effects on generating IGF-l, decreasing ROS, improving kidney function and its effect on the generation of the vasodilator nitric oxide [NO]. The present study included four groups of albino rats, the first group [control group] was injected with saline, the second group [AFR group], in which 50% of glycerol was injected intramuscularly [im]. The third group was injected with the vehicle of growth hormone and the fourth group was injected with rh-GH [2 mg/day] for 5 days subcutaneously [sc] 48 hr after induction of ARF. The results showed 3.79 and 4.09 folds increase in blood urea and serum creatinine, respectively for the ARF group compared to the control group. These values in group IV deceased by 79.5 and 49% after rh-GH hormone treatment compared to their controls [group III]. Also the increased mean value of plasma malondialdehyde [MDA] and deceased mean value of plasma nitric oxide [NO] in the ARF group as compared to controls were markedly corrected after rh-GH treatment. The greatly increased level of IGF-l after rh-GH injection suggests that it may be the actual player behind these ameliorating effects of rh-GH on glycerol-induced ARF in rats. The therapeutic uses of rh-GH in ameliorating the effects of ARF that has already happened [as early as possible] and its protective effects in expected cases is therefore recommended

Role of oxytocin as regulator of leptin secretion and its relation to biochemical markers [OPG and SRANKL] of bone resorption and formation

Increasing evidences demonstrated many new targets for the hypothalamic hormone oxytocin [OT] supporting the presence of a central neuroendocrine and/or humoral factors that control bone remodeling. The present study was carried out to test the effect of OT on serum leptin level and on the regulation of skeletal homeostasis through measurement of serum levels of osteoprotogerin OPG [secreted glycoprotein of the tumour necrosis receptor superfamily], sRANKL [soluble decoy receptor activator of nuclear factor kappa filigand], calcium and phosphorus. Fifty adult male albino rats used in this study. They were divided into three groups: group I which was subdivided into 3 subgroups, subgroup IA untreated control, IB injected with DM SO [0.16 ml/kg, b.wt x 6 weeks], 1C injected with DMSO [0.08 ml/kg b.wt for 12 weeks]. II OT treated [40 micro/kg b.wt x6 weeks] group. Ill OT [8 micro/kg b.wt x 12 weeks] group. The results obtained showed very high significant increase in OPG level in group [II] compared with subgroups I A and IB and high significant increase of OPG in group [III] compared with subgroup 1C. On the other hand, non significant change was detected in serum levels of sRANKL. As regards serum leptin, a high significant increase was found in group II as compared with subgroups IA and IB and a high significant increase was detected in group [III] compared with IA and 1C subgroups. Serum calcium and phosphorus levels showed very high significant decrease in group [II] compared with IA and IB subgroups and high significant decrease in group [HI] compared with subgroup IA. Also, significant increase in OPG/sRANKL ratio in group [II] compared with IA subgroup. A negative correlation between sRANKL and OPG/sRANKL ratio was obtained in both OT treated groups.The OPG and sRANKL levels obtained in OT treated rats favor increased osteoblast over osteoclast activity and may explain, in part, the imbalance in bone remodeling in favor of bone formation. 'The rise in OPG serum level is probably a homeostatic mechanism to limit bone loss. We can say that leptin should be reappraised as an indicator of energy supplies available for homeostasis, which now includes bone remodeling. We can conclude that the stimulating effect of OT on serum leptin together with increased OPG synthesis indicate anabolic effect on osteoblastic cells to support bone formation and indicate the important role of OPG in bone remodeling and it may be useful for the treatment of osteoporosis associated with increased osteoclast function. OT and leptin can now be added to the array of bone modulating signalling molecules