Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Optic nerve hypoplasia is seen in 50% of patients diagnosed with fetal alcohol syndrome and is due to a defect in the development of retinal ganglion cells. Somatostatin may influence the development of retinal ganglion cells, so we studied the effect of in vivo ethanol exposure on somatostatin expression in the developing retina. Somatostatin concentration is increased in retina from ethanol-exposed fetuses and pups and this increase in peptide is associated with excessive neurite formation and improper migration of the somatostatin-containing neurons at early postnatal ages. These disturbances may account for the eventual failure in retinal ganglion cell development that results in optic nerve hypoplasia.
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PMID:Somatostatin is altered in developing retina from ethanol-exposed rats. 136 62

Ethanol exposure on gestational day (GD) 7 in the mouse has previously been shown to result in ventromedian forebrain deficits along with facial anomalies characteristic of fetal alcohol syndrome (FAS). To further explore ethanol's teratogenic effect on the ventromedian forebrain in this mouse model, scanning electron microscopic and histological analyses were conducted. For this, time mated C57Bl/6J mice were injected with 2.9g/kg ethanol or saline twice, at a 4h interval, on their 7th day of pregnancy. On GD 12.5, 13 and 17, control and ethanol-exposed specimens were collected and processed for light and scanning electron microscopic analyses. Gross morphological changes present in the forebrains of ethanol-exposed embryos included cerebral hemispheres that were too close in proximity or rostrally united, enlarged foramina of Monro, enlarged or united lateral ventricles, and varying degrees of hippocampal and ventromedian forebrain deficiency. In GD 12.5 control and ethanol-exposed embryos, in situ hybridization employing probes for Nkx2.1 or Fzd8 to distinguish the preoptic area and medial ganglionic eminences (MGEs) from the lateral ganglionic eminences, respectively, confirmed the selective loss of ventromedian tissues. Immunohistochemical labeling of oligodendrocyte progenitors with Olig2, a transcription factor necessary for their specification, and of GABA, an inhibitory neurotransmitter, showed ethanol-induced reductions in both. To investigate later consequences of ventromedian forebrain loss, MGE-derived somatostatin-expressing interneurons in the subpallial region of GD 17 fetal mice were examined, with results showing that the somatostatin-expressing interneurons that were present were dysmorphic in the ethanol-exposed fetuses. The potential functional consequences of this insult are discussed.
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PMID:Ventromedian forebrain dysgenesis follows early prenatal ethanol exposure in mice. 2107 10

In addition to regulate body growth and development process, growth hormone (GH) also involved in lipid metabolism, decreasing fat mass and improving lipolysis. To normal mice, GH could reduce their fat content, but events turned uncertain coming to the pattern of feeding high-fat-diet. In order to investigate the role of GH in adipogenesis of mice with high-fat-diet, the high-fat-diet feeding mice were randomly assigned into three groups and treated with recombinant human growth hormone (rhGH) and the somatostatin analogue octreotide respectively. Results demonstrated that both rhGH and octreotide could reduce the body weight but the trends diminished in the end. HDL-C level was increased in octreotide treated groups but the activity of lipase was increased significantly in both two groups. RhGH remarkable increased the expression of SOCS2, FAS (P < 0.01) and SREBP-1c (P < 0.05), decreased the expression of SOCS1, SOCS3 (P < 0.05) and HSL (P < 0.01) in subcutaneous fat mass. In visceral fat tissue, all genes were increased except SOCS2 (P < 0.01), at the same time the visceral fat mass was decreased. The protein phosphorylation of JAK2 and STAT5 which were treated with octreotide were increased in subcutaneous fat, visceral fat and liver (P < 0.01) and were increased significant in visceral fat by rhGH treated (P < 0.01). In liver, only JAK2 protein phosphorylation was raised (P < 0.01). In conclusion, rhGH and octreotide could decrease the whole body mass before 6 days; the trend was weaken in later period with high-fat-diet. RhGH could increase the subcutaneous fat mass and reduce the visceral fat mass, and SOCS2 might be involved in regulation of the mechanism through JAK2/STAT5 signaling pathway.
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PMID:The role of SOCS2 in recombinant human growth hormone (rhGH) regulating lipid metabolism in high-fat-diet-induced obesity mice. 2318 49