Effects of exogenous ghrelin on the tissue structure and somato-statin secretion in the pancreas of African ostrich chicks / Efectos de la grelina exógena en la estructura del tejido y la secreción de somato-estatinas en el páncreas de los polluelos de avestruz africanos

SUMMARY: This study aimed to investigate the effect of exogenous ghrelin on pancreatic growth and development in African ostrich chicks. Sixteen 40-day-old African ostrich chicks (male or female) were randomly divided into four groups and injected intravenously metatarsal vein with saline (control) or ghrelin (10, 50, and 100 μg/kg) for 6 days. Body and pancreas weight were determined, structural characteristics were observed using HE staining, somatostatin-immunopositive cells were detected using immunohistochemistry. The results were as follows: 1. The 50 and 100 μg/kg groups showed lower relative pancreas weight than the control group (P 0.05. Moreover, compared with the control, the islet cells in treatment groups were loosely arranged and showed reduced cytoplasm. In the exocrine pancreas, the volume of acinar cells in the 10, 50, and 100 μg/kg groups all decreased to varying degrees. 3. Somatostatin immunopositive cells were mainly located around the periphery of the islets and sporadically distributed in the center. The density of the somatostatin immunopositive cells in the 10, 50, and 100 μg/kg groups was higher than that in the control (P < 0.05). These findings suggest that exogenous ghrelin increases the area and number of islets and number of somatostatin immunopositive cells but reduces relative pancreas weight and effects the morphological and structural development of the pancreas, which may inhibit the pancreatic growth and development in African ostrich chicks.

RESUMEN: Este estudio tuvo como objetivo investigar el efecto de la grelina exógena sobre el crecimiento y desarrollo del páncreas en polluelos de avestruz africana. Dieciséis pollos de avestruz africana de 40 días (machos o hembras) se dividieron al azar en cuatro grupos y se inyectaron por vía intravenosa con solución salina (control) o grelina (10, 50 y 100 μg / kg) durante 6 días. determinadas, se observaron las características estructurales mediante tinción Hematoxilina-Eosina, se detectaron células inmunopositivas a somatostatina mediante inmunohistoquímica. Los resultados fueron los siguientes: ¨Los grupos de 50 y 100 μg / kg mostraron un menor peso relativo del páncreas que el grupo de control (P <0,05). El área de islotes por unidad de área del páncreas fue mayor en los grupos de 10, 50 y 100 μg / kg grupos que en el grupo de control (P <0,05). El número de islotes por unidad de área del páncreas fue menor en el grupo de 10 μg / kg que en el control (P <0,05). Además, en comparación con el control, las células de los islotes en los grupos de tratamiento estaban dispuestas de forma holgada y mostraban un citoplasma reducido. En el páncreas exocrino, el volumen de células acinares en los grupos de 10, 50 y 100 μg / kg disminuyó en diversos grados. Las células inmunopositivas de somatostatina se ubicaron principalmente alrededor de la periferia de los islotes y se distribuyeron esporádicamente en el centro. La densidad de las células inmunopositivas a la somatostatina en los grupos de 10, 50 y 100 μg / kg fue mayor que la del control (P <0,05). Estos hallazgos sugieren que la grelina exógena aumenta el área y el número de islotes y el número de células inmunopositivas a la somatostatina, pero reduce el peso relativo del páncreas, lo que puede inhibir el crecimiento y desarrollo pancreático en los polluelos de avestruz africana.

Regulation of glucagon, somatostatin and GLP-1 by insulin and forskolin in rats

Glucagon had stimulatory effect on insulin secretion and insulin inhibits glucagon release. The possible mechanism of insulin effect on proglucagon gene transcription under physiological conditions has to be established. Conflicting reports exist regarding signal pathway involved in the regulation of islet and intestinal glucagon producing cells, therefore, present study was designed to determine the in-vivo effect of insulin and forskolin on glucagon. Design: Prospective and experimental study. Place and Duration of Study: The study was conducted in the Department of Chemical Pathology and Endocrinology, Armed Forces Institute of Pathology, Rawalpindi. Laboratory facilities of the Department of Metabolic Medicine, Hammersmith Hospital, London were used for specialized procedures. The study was completed in one year. Subjects and An in-vivo study was conducted by producing hyperinsulinaemic, isoglycaemic clamp. Forskolin, which is a direct activator of adenylate cyclase system, was infused to diabetic rats to establish the second messenger involved in the regulation of islets cell function and intestinal glucagon gene transcription. Insulin decreased glucagon secretion and its mRNA in rats infused with insulin as compared to controls. Plasma levels of glucagon was more in diabetic as compared to non diabetic control rats. It is interpreted that glucagon mRNA in diabetic controlled rats will also be more as compared to normal controlled rats. GLP-1 level in diabetic controls was more as compared to non diabetic controls indicating loss of inhibitory effect on intestinal glucagon by insulin in diabetics. Insulin infusion significantly decreased GLP-1 levels in diabetic rats. Forskolin did not affect the glucagon secretion or its mRNA in pancreas but it increased GLP-1 levels in plasma of rats. Somatostatin levels decreased by insulin and a significant hypersomatostatinemia was observed in diabetic controls as compared to non diabetic control rats. Forskolin increased somatostatin and insulin secretions. Concentrations of insulin were significantly high [about 10 times] as compared to controls in rats infused with insulin. It is concluded that insulin normalizes hyperglucagonemia in diabetics by exerting its effects at gene transcription level. Insulin also negatively regulates intestinal proglucagon gene. Somatostatin is negatively regulated by insulin. The cAMP dependent pathway may be involved in the regulation of glucagon gene in intestine. Pancreatic B and D cells are stimulated by cAMP dependent pathway. The increased insulin, somatostatin and GLP-1 in response to forskolin may have masked the effect of forskolin on A cells, due to which no effect on glucagon secretion and synthesis was observed

Regulation of glucagon gene expression by insulin

To study the effects of 10e-6 and 10e-7 M exogenous insulin [the concentrations which correspond to insulin concentrations in core capillaries of islets in-vivo] on glucagon gene regulation in intact islets in RPMI 1640 culture medium. Design: An experimental study. Place and Duration of Study: The study was carried out in the Department of Chemical Pathology and Endocrinology, Armed Forces Institute of Pathology, Rawalpindi and the Department of Metabolic Medicine, Hammersmith Hospital, London from 1995 to 1996. Subjects and Wistar rats were used to obtain visible islets from pancreas by collagenase degradation of exocrine tissue. The effect of 10-s and 10- M insulin was observed on glucagon and insulin mRNA and glucagon, Insulin and somatostatin secretions in the culture medium at the end of 18 hours of incubation. Insulin decreased glucagon levels in culture medium [366.7 +/- 42.9 in 10e-6 M insulin vs 450 +/- 38.9 in controls; p < 0.01]. No significant effect on glucagon secretion by 10-7 M insulin was observed. Reduction of glucagon mRNA by insulin was also observed [77.8 +/- 30.3 in 10e-6 and 94.5 +/- 15.6% control in 10e-7 M insulin]. Somatostatin secretions decreased in culture medium by 10e-6 and 10e-7 M insulin as compared to controls [103.6 +/- 16.4 in 10e-6 M insulin and 115.4 +/- 7.4 in 10e-7 M insulin vs 166.6 +/- 19.9 in control islets, p <0.001]. Insulin mRNA was inhibited by insulin [91.5 +/- 35.4 in 10e-6 M insulin and 94.8 +/- 19% controls in 10e-7 M insulin]. Concentrations of insulin were significantly high as compared to controls in medium of islets treated with 10e-6 M insulin [107876 +/- 5837 in 10e-6 M insulin vs 57205 +/- 8392 in control islets, p <0.001]. No significant difference in insulin levels in medium existed in 10e-7 M insulin as compared to control islets. It is concluded that insulin normalizes hyperglucagonemia in diabetics by exerting its effects at gene transcription level and somatostatin is negatively regulated by insulin

Effect of eradication of Helicobacter pylori, using omeprazole and amoxicillin, on the level of serum gastrin, somatostatin and secretin in Egyptian patients with duodenal ulcers

Forty-three patients with duodenal ulcer [DU] diagnosed by endoscopy and fifty-one patients with non-ulcer dyspepsia [NUD] were included in this study. The diagnosis of H. pylori [HP] was performed using urease test and culture of four biopsies from the antrum and corpus. Gastrin was measured by RIA, SO and SEC by ELISA. DUs patients received omeprazole [20 mg/day] for four weeks and amoxicillin [500 mg 3 times/day] for two weeks and follow up was performed for 23 patients with DUs after one month. It was concluded that patients with DUs had higher levels of G and lower levels of SO and SEC than patients with NUD. HP seems to be responsible for increased G and reduced SO in patients with DUs and its eradication led to significant reduction of G and increase in SO with consequent reduction in acid secretion

Somatostatina por via epidural em ratos: efeito sobre a transmissao da dor / Effect of epidural somatostatin on pain transmission in rats

Foram avaliados os efeitos da somatostatina-201-995 por via epidural sobre a transmissao da dor em ratos.Os ratos do G-I(10)receberam salina; os do G-II, 10 mcg de SST; os do G-III, 30 mcg de SST. O volume foi de 40mcl. A SST nao alterou a resposta a dor (imersao em agua quente). Houve efeitos colaterais em cinco ratos.

Different effects of pyridostigmine on growth hormone (GH) response to GH-releasing hormone in endogenous and exogenous hypercortisolemic patients

1. Somatostatin may play a role in the inhibition of growth hormone (GH) response to GH-releasing hormone (GHRH) in hypercortisolism. To examine this hypothesis we studied the effect of pyridostigmine, a cholinergic agonist that decreases hypothalamic somatostatin, on the GH response to GHRH in 8 controls, in 6 patients with endogenous hypercortisolism (3 with Cushing's disease and 3 with adrenal adenomas) and in 8 patients with exogenous hypercortisolism (lupus erythematosus chronically treated with 20-60 mg/day of prednisone). Each subject received GHRH(1-29)NH2,100 micrograms iv twice, preceded by pyridostigmine (120 mg) or placebo, orally. 2. The GH response to GHRH was significantly blunted in all hypercortisolemic patients compared to controls both after placebo (GH peak, 5.8 +/- 1.6 vs 46.2 +/- 15.9 micrograms/l, mean +/- SEM) and after pyridostigmine (15.7 +/- 5.6 vs 77.2 +/- 19.8 micrograms/l). 3. The GH response was absent in endogenous hypercortisolemic patients compared to the exogenous group, both after placebo (2.2 +/- 0.3 vs 8.5 +/- 2.4 micrograms/l) and after pyridostigmine (4.9 +/- 2.5 vs 23.8 +/- 8.7 micrograms/l). The GH release after GHRH/pyridostigmine for the exogenous group was similar to the response of controls treated with GHRH/placebo. 4. These results confirm that the GH response to GHRH is blunted in hypercortisolism, although more pronounced in the endogenous group. Pyridostigmine partially reversed this inhibition in the exogenous group. Therefore, somatostatin may play a role in the inhibition of GHRH-induced GH release in exogenous hypercortisolemic states

Estudo comparativo da atividade da somatostatina sobre a hemodinâmica portal, tanto em cachorros normais como em portadores de um modelo misto de hipertensao portal / Comparative study of the somatostatin activity on the portal hemodynamics, both in normal dogs or portal hypertensive dogs

Realizamos um modelo experimental de hipertensao portal crônica em cachorros. A hipertensao portal foi obtida através de dois mecanismos: 1) aumento do fluxo portal por meio de uma anastomose cavo-portal término-lateral; 2) obstruçao extra-hepática progressiva distal a anastomose, utilizando um anel de constriçao progressiva. Após, estudamos os efeitos da somatostatina na pressao portal dos cachorros que utilizaram nosso modelo e comparamos com o grupo de controle de cachorros normais.