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)

Previous studies have shown that patients with chronic alcohol ingestion may show a variety of morphological and functional alterations in the small intestine. In this study, we have focused on the neuroendocrine system in the duodenal mucosa in chronic alcoholics; an area little studied. Twenty-three defined chronic alcoholics admitted to the hospital for detoxification underwent clinical examination, followed by upper gastrointestinal endoscopy and blood tests on average 4 days after the most recent alcohol intake. Biopsy specimens were taken from the distal part of the descending duodenum for both immunohistochemical and routine histological examination. The control group consisted of 25 patients referred for upper endoscopy mainly because of dyspepsia (ulcer, reflux type), but who were otherwise healthy. A normal carbohydrate-deficient transferrin and a history of low alcohol consumption (<40 g/week) were required for inclusion in the control group. The tissue specimens were studied using antisera for the following neuropeptides: cholecystokinin, galanin, gastric inhibitory peptide (GIP), glucagon, motilin, neuropeptide Y, pituitary adenylyl cyclase activating peptide, secretin, serotonin, somatostatin, substance P, vasoactive intestinal polypeptide and protein gene product, as a general marker for neurones and cells of the diffuse neuroendocrine system. The density of nerve fibres was evaluated semi-quantitatively and the number of endocrine cells per unit length of mucosa was counted in sections cut perpendicularly to the mucosal surface. All the different peptidergic nerve fibres in the alcohol group showed higher densities than the corresponding controls. However, this was not a statistically significant difference. A slightly significant increase (P = 0.02) in the numbers of glucagon and GIP cells was seen in the alcohol group. Gastrointestinal symptoms were frequently present (87%) in chronic alcoholics. We suggest that chronic alcohol consumption in man may have a general effect on the peptidergic nerve system and some endocrine cell types in the duodenal mucosa.
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PMID:Neuropeptides in the duodenal mucosa of chronic alcoholic heavy drinkers. 1137 57

Though sex steroids are found to influence thyroid pathogenesis in human and in animals, their role in normal thyroid growth and thyrocyte proliferation is not yet understood fully. The present study is addressed to know the effect of testosterone and estradiol on the basal and TSH-induced thyrocyte proliferation in immature and adult rats in vitro. The male and female Wistar rats were gonadectomized (GDX) and one group of GDX rats were supplemented with either testosterone or estradiol. After the experimental period, the rats were sacrificed by decapitation and thyroid glands were removed, washed in Hank's Balanced Salt Solution (HBSS), pH 7.4 and digested with the enzyme mixture containing 0.08% collagenase and 0.12% dispase in HBSS. The isolated follicles were washed thrice with Dulbecco's modified Eagle's medium (DMEM) containing 0.5% fetal bovine serum (FBS), and were cultured in Falcon's tissue culture flasks containing 5 ml DMEM with FBS (5%) transferrin (5 microg/ml), hydrocortisone (10(-8) M), somatostatin (10 microg/ml), insulin (10 microg/ml) and glycyl-L-histidyl-L-lysine acetate (10 microg/ml). The cells (2.5 x 10(4)) were exposed to various exponential doses of TSH or testosterone (6.25-800 ng/ml) or estradiol (6.25-800 pg/ml). It is suggested from the present study that both TSH and sex steroids enhance thyrocyte proliferation. The mitogenic effect of TSH is greater than that of sex steroids. Sex steroids modulate TSH-induced cell proliferation in a gender-specific manner.
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PMID:Testosterone and estradiol differentially regulate TSH-induced thyrocyte proliferation in immature and adult rats. 1199 29

The long-term culture of functional follicular cells from normal adult human thyroid tissue has been obtained. They were expanded using a 1:2 split ratio until passage 28 (present status) in Click-RPMI medium enhanced with 5% fetal calf serum and diverse associations of hormones or components including porcine insulin and bovine thyrotropin. At passages 10 and 20, chromosome countings showed a normal diploid number and a normal karyotype. In calf serum containing media, cells are epithelial in the presence of thyrotropin (TSH) but present a slight elongated form in the absence of TSH. In serum-free media, 30 minutes after TSH stimulation, both epithelial and elongated cells changed in morphology to stellate-shaped, arborized forms, indicating the presence of functional TSH-receptors even in long term (18 months) TSH-free cultures. Cells produce thyroglobulin constitutively and large amounts of thyroglobulin are easily recovered in TSH-supplemented media, especially in the presence of insulin. Thyroglobulin production was increased versus days under TSH or insulin stimulation. Combination of the two hormones clearly resulted in a synergistic and not an additive effect. The other hormones present in the 6H components (transferrin, glycylhistidyl-lysine, somatostatin, and hydrocortisone) had no positive effect on thyroglobulin accumulation in media in our experimental conditions. Addition of TSH to hormone-free cultures or to insulin-, insulin plus hydrocortisone-, or 5H-containing cultures resulted in a clear increase in thyroglobulin production. Withdrawal of TSH from 6H cultures resulted in a decrease in thyroglobulin accumulation in media. Six months were required to select fibroblast-free cultures and to get passage 6. But only 17 months separated passage 6 to passage 28, indicating that the proliferative rate is increasing with in vitro cell adaptation. Such normal adult thyroid cells, thyroglobulin-producing, TSH, and insulin-sensitive, represent a new normal human thyroid cell line allowing comparative studies with cells originating from pathologic thyroid tissues.
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PMID:Isolation of a normal human thyroid cell line: hormonal requirement for thyroglobulin regulation. 1219 96

Type I diabetes mellitus is caused by an autoimmune destruction of the insulin-producing beta cells. The major obstacle in using transplantation for curing the disease is the limited source of insulin-producing cells. The isolation of human embryonic stem (hES) cells introduced a new prospect for obtaining a sufficient number of beta cells for transplantation. We present here a method for forming immature islet-like clusters of insulin-producing cells derived from hES cells. The protocol consisted of several steps. Embryoid bodies were first cultured and plated in insulin-transferrin-selenium-fibronectin medium, followed by medium supplemented with N2, B27, and basic fibroblast growth factor (bFGF). Next, the glucose concentration in the medium was lowered, bFGF was withdrawn, and nicotinamide was added. Dissociating the cells and growing them in suspension resulted in the formation of clusters which exhibited higher insulin secretion and had longer durability than cells grown as monolayers. Reverse transcription-polymerase chain reaction detected an enhanced expression of pancreatic genes in the differentiated cells. Immunofluorescence and in situ hybridization analyses revealed a high percentage of insulin-expressing cells in the clusters. In addition to insulin, most cells also coexpressed glucagon or somatostatin, indicating a similarity to immature pancreatic cells. Further improvement of this insulin-producing cell protocol may lead to the formation of an unlimited source of cells suitable for transplantation.
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PMID:Differentiation of human embryonic stem cells into insulin-producing clusters. 1515 4

Ascorbic acid (AA) has been shown to increase the yield of dopaminergic (DA) neurons derived from basic fibroblast growth factor (bFGF)-expanded mesencephalic precursors. To understand the molecular mechanisms underlying this phenomenon, we used cDNA microarray analysis to examine differential expression of neuronal genes following AA treatment. The putative precursor cells were isolated from E13 rat ventral mesencephalons and expanded in the presence of bFGF. Cells were incubated in mitogen-free media supplemented with 200 microM AA or were left untreated as a control, and total RNA was isolated at different time points (expansion stage and 1, 3, and 6 days after induction of differentiation) and subjected to cDNA microarray analysis. Differentiation was evaluated by Western blot analysis and immunocytochemistry of neuron-specific markers. AA treatment of the mesencephalic precursors increased the expression of neuronal (MAP2) and astrocytic (glial fibrillary acidic protein) markers and the percentage of tyrosine hydroxylase (TH)-positive cells. The microarray analysis revealed that 12 known genes were up-regulated and 20 known genes were down-regulated in expansion-stage AA-treated cells. Six days after the induction of differentiation, AA-treated cells showed up-regulation of 48 known genes and down-regulation of 5 known genes. Our results identified several proteins, such as transferrin, S-100, and somatostatin, as being differentially regulated in AA-treated mesencephalic precursors. This novel result may lead to a better understanding of the molecular mechanisms underlying the AA-induced differentiation of mesencephalic precursors into DA neurons and may form the basis for improved DA neuronal production for treatment of Parkinson's disease patients.
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PMID:Changes of gene expression profiles during neuronal differentiation of central nervous system precursors treated with ascorbic acid. 1537 4


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