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)

Basal and postprandial concentrations of gastrointestinal hormones were measured in 12 dogs before and at one and three months after a 75% small bowel resection. Five animals were studied again at six months. Concentrations of enteric hormones and neuropeptides, measured in the proximal jejunum and distal ileum adjacent to the anastomotic site at the time of euthanasia, were compared with concentrations in control tissues taken from each animal at the time of resection. Increased basal and postprandial levels of gastrin (P < 0.05), cholecystokinin (CCK, P < 0.05), glucose-dependent insulinotropic peptide (GIP, P < 0.01), peptide YY (PYY, P < 0.001), and enteroglucagon (P < 0.001), were seen at one month after small bowel resection. In contrast, no significant changes were seen in concentrations of secretin, motilin, neurotensin, somatostatin, PP, or glucagon. Concentrations of enteroglucagon, GIP, and PYY remained high throughout the six-month study period. In contrast, gastrin and CCK had normalized by three months. Thus, only enteroglucagon, PYY, and GIP showed sustained elevations following enterectomy; the gastrin and CCK changes were transient. Following enterectomy, concentrations of vasoactive intestinal polypeptide (VIP) were reduced by about 50% in mucosal (P < 0.001) and muscle (P < 0.05) layers of proximal and distal gut. In contrast, calcitonin gene-related peptide (CGRP) was increased by about twofold in jejunal and ileal mucosa (P < 0.05), and CGRP elevations were even more marked in the muscle layers (P < 0.001). Somatostatin and neuropeptide Y (NPY) concentrations were similar to controls in all areas except for a small decrease in NPY in ileal mucosa (P < 0.05). These findings suggest that the increased motilin and PP concentrations previously reported after bowel resection in man are more likely to reflect underlying inflammatory bowel disease rather than enterectomy. The normalization of hypergastrinemia explains why the increased acid secretion after small bowel resection is transient. These results provide evidence for independent secretory control of enteroglucagon and PYY, which are both products of intestinal L cells. In addition, these studies reveal marked changes in enteric neuropeptide concentrations following bowel resection. VIP, which is thought to be a major inhibitory transmitter in the gut, is markedly reduced, while CGRP, which is mainly localized in sensory afferent fibers, is increased. These major neuropeptide changes are likely to be of importance in the adaptive responses to massive small bowel resection.
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PMID:Time course of adaptive regulatory peptide changes following massive small bowel resection in the dog. 865 52

High-resolution capacitance measurements were used to explore the effects of the gut hormones GLP-I(7-36) amide [glucagon-like peptide I(7-36) amide] and GIP (glucose-dependent insulinotropic polypeptide) on Ca2+-dependent exocytosis in glucagon-secreting rat pancreatic alpha-cells. Both peptides produced a greater than threefold potentiation of secretion evoked by voltage-clamp depolarizations, an effect that was associated with an approximately 35% increase of the Ca2+ current. The stimulatory actions of GLP-I(7-36) amide and GIP were mimicked by forskolin and antagonized by the protein kinase A (PKA)-inhibitor Rp-8-Br-cAMPS. The islet hormone somatostatin inhibited the stimulatory action of GLP-I(7-36) amide and GIP via a cyclic AMP-independent mechanism, whereas insulin had no effect on exocytosis. These data suggest that the alpha-cells are equipped with receptors for GLP-I and GIP and that these peptides, in addition to their well-established insulinotropic capacity, also stimulate glucagon secretion. We propose that the reported inhibitory action of GLP-I on glucagon secretion is accounted for by a paracrine mechanism (e.g., mediated by stimulated release of somatostatin that in turn suppresses exocytosis in the alpha-cell).
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PMID:Glucagon-like peptide I and glucose-dependent insulinotropic polypeptide stimulate Ca2+-induced secretion in rat alpha-cells by a protein kinase A-mediated mechanism. 913 46

Histological, immunocytochemical and immunofluorescence methods were employed to study the intestine and endocrine pancreas of the elephant. The histological findings were in line with those in monogastric mammals. In the mucosa of intestine, endocrine cells were immunoreactive to somatostatin, gastrin, CCK, GIP, secretin, motilin, glucagon and NPY. Nerve cells immunoreactive to somatostatin, substance P, VIP, PHI, NPY, bombesin and CGRP were detected. No immunoreactivity to neurotensin was observed, islets of the pancreas had insulin cells in their cores and glucagon and somatostatin cells in their mantles. The antisera employed failed to demonstrate PP cells in the pancreas, but NPY-immunoreactive cells were present.
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PMID:The intestine and endocrine pancreas of the African elephant: a histological immunocytochemical and immunofluorescence study. 917 65

Co-localization of chromogranin (Cg) A, B, and C has been studied in different neuroendocrine cell types in histologically normal mucosa from human gastrointestinal tract (corpus, antrum, duodenum, ileum, and colon) using single-, double-, and triple-immunofluorescence stainings. Virtually all enterochromaffin (EC) cells contained CgA, and those in the luminal two thirds of the antral mucosa and villi of small intestine often also contained CgB. A few EC cells in the duodenal crypts contained CgC. Most gastrin cells harbored both CgB and CgA, although rather more CgB than CgA, but some gastrin cells contained all three types, i.e., also CgC. Some CCK cells also contained all three chromogranins. Enteroglucagon cells in the duodenal villi contained CgA and some CgB. CgA (but not B or C) was found in some secretin, GIP, enteroglucagon/peptide YY, and neurotensin cells. A few somatostatin cells contained CgA but neither CgB nor CgC. CgA and C were found mainly in the basal cell region, whereas CgB occurred more diffusely throughout the cytoplasm. This varying distribution suggests that not all secretory granules contain CgA, or that CgB may occur in a nongranular form. The varying composition of the different chromogranins may reflect their complex functional roles in the widespread neuroendocrine system.
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PMID:Complex co-localization of chromogranins and neurohormones in the human gastrointestinal tract. 919 67

The endocrine cells in the duodenum of pre-diabetic and diabetic female non-obese diabetic (NOD) mice aged 22-24 weeks were studied by means of immunohistochemistry and computed image analysis as well as by radioimmunoassays of tissue extracts. As controls, 12 female BALB/cJ mice of the same age as NOD mice were used. The number of secretin-immunoreactive cells increased in diabetic but not in pre-diabetic NOD mice. The level of extractable secretin was higher in both pre-diabetic and diabetic NOD mice. The number of GIP-, CCK/gastrin-, and serotonin-immunoreactive cells was significantly reduced in both pre-diabetic and diabetic NOD mice. There was no statistical difference in the number of somatostatin-immunoreactive cells between the NOD mice and controls. The level of GIP was higher and gastrin was lower in NOD mice compared to controls. There was no statistical difference in the somatostatin level between the NOD mice and controls. The cell secretory index was elevated in all the endocrine cell types except CCK/gastrin cells. It has been suggested that some of the changes in the duodenal endocrine cells could be attributed to the diabetes state, but most of the changes seem to take place before the onset of diabetes. The abnormalities in the duodenal endocrine cells observed here in an animal model for diabetes type I might have relevance for the gastrointestinal dysfunction displayed in human diabetes.
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PMID:Abnormalities of small intestinal endocrine cells in non-obese diabetic mice. 964 40

Coeliac disease is associated with intestinal lesion. This lesion causes architectural derangement of the mucosa in the form of villus atrophy, increased crypt length and increased volume of the lamina propria. Several changes in the intestinal endocrine cells have been reported over the years, e.g. the number of secretin cells and increased numbers of GIP, CCK/gastrin, motilin, and serotonin cells. There is no consensus about the nature of the changes in somatostatin-cells. It has been postulated that the changes in the endocrine cells are a selective process to meet the new demands exerted by the dramatic decrease in intestinal absorptive area. It has been speculated further that the changes in the endocrine cells would cause an incomplete digestion of the ingested food and its rapid elimination from the intestine. These changes may be responsible for the diarrhoea and steatorrhoea that occur in patients with coeliac disease.
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PMID:The nature and implication of intestinal endocrine cell changes in coeliac disease. 981 May 3

1. The effect of a new type 2 selective somatostatin (SRIF) receptor antagonist (DC-41-33) on somatostatin-induced inhibition of pentagastrin-stimulated gastric acid secretion in conscious, chronic gastric fistula equipped rats was studied. 2. Infused intravenously, DC-41-33 dose-dependently inhibits SRIF-induced inhibition of pentagastrin-stimulated gastric acid secretion with an IC50 of 31.6+/-1.2 nmol kg(-1) versus 10 nmol kg(-1) SRIF and blocks the inhibitory effects of SRIF when simultaneously co-infused. Its effectiveness provides additional evidence that SRIF-inhibition of gastric acid release is a SRIF type 2 receptor-mediated process. 3. DC-41-33 is able to completely reverse the inhibitory effect of glucose-dependent insulinotropic polypeptides, GIP and GIP-(1-30)NH2, and glucagon-like polypeptide, GLP-1(7-36)NH2, on pentagastrin-stimulated gastric acid secretion thus confirming that they exert these effects through stimulation of endogenous SRIF release. 4. DC-41-33 only partially blocks potent amylin and adrenomedullin-induced inhibition of gastric acid secretion, therefore suggesting that somatostatin may not function as a primary mediator in the action of these peptides. 5. Our results indicate that DC-41-33, is a potent in vivo inhibitor of exogenous and endogenous SRIF in rats. It represents a new class of SRIF analogues which should eventually provide excellent tools for further evaluating the many physiological roles of SRIF and its five receptor subtypes.
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PMID:Examination of somatostatin involvement in the inhibitory action of GIP, GLP-1, amylin and adrenomedullin on gastric acid release using a new SRIF antagonist analogue. 984 48

The effect of right or left unilateral cervical vagotomy on the intestinal endocrine cells was studied in 23 mice at 2 and 8 weeks after operation, respectively. The results were compared with that from 10 sham operated mice. Various types of endocrine cells in duodenum and proximal colon were detected by immunohistochemistry and quantified by computerized image analysis. In mouse duodenum, chromogranin-, CCK/gastrin-, GIP- and somatostatin-cells were significantly decreased at 2 weeks after right vagotomy, but returned to the control levels at 8 weeks. Serotonin-cells were reduced at both 2 and 8 weeks after right vagotomy. The amount of the duodenal endocrine cells did not change after left vagotomy with the exception of secretin-cells, which were diminished at 8 weeks after both right and left vagotomy. In the proximal colon, chromogranin-cells were also decreased at 2 weeks after right vagotomy. Serotonin-cells were reduced at 8 weeks after left vagotomy but not right vagotomy. There was no significant difference between the unilaterally vagotomized and the sham operated mice with regard to PYY- and glucagon-cells. It was concluded that vagotomy affected the intestinal endocrine cells in mouse. The influence was more pronounced in the small intestine than the proximal colon. The right vagus nerves seemed to exert more effect on the intestinal endocrine cells than the left ones.
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PMID:Changes in intestinal endocrine cells in the mouse after unilateral cervical vagotomy. 1021 6

The aim of this study was to quantify the effect of oral refeeding on the synthesis of soluble and contractile proteins in skeletal muscles, and to evaluate to what extent diet components (carbohydrate, fat, amino acids), hormones (insulin, IGF-I, GIP), Ca2+ flux, polyamine synthesis, cyclooxygenase activity, and muscle innervation are related to activation of protein synthesis at the translational level following oral refeeding. Adult, weight-stable, non-growing mice (C57B1) were used in starvation/refeeding experiments with oral chow. Growing rats (150 g) were used in parenteral refeeding experiments. Protein synthesis was measured in vivo in mixed muscles (phenylalanine flooding), in phasic EDL muscles (in vitro), and in cultured L-6 muscle cells. Overnight starvation reduced synthesis of soluble proteins by 37 +/- 8% (from 0.242 +/- 0.025 to 0.151 +/- 0.009 microgram-1.mg-1) and contractile proteins by 55 +/- 6% (from 0.148 +/- 0.018 to 0.068 microgram-1.mg-1) (P < 0.01). Soluble proteins with a basic net charge were more sensitive to nutrition compared to neutral and acidic proteins. Somatostatin treatment before refeeding attenuated muscle protein synthesis by 15% (P < 0.02). Mechanical stimulation of the gastrointestinal tract (bulk feeding) did not activate protein synthesis in muscles, while i.v. or i.p. provision of nutrients did. Oral refeeding normalized rates of protein synthesis within 3 h (P < 0.01), independently of intact muscle innervation, Ca2+ flux, polyamine synthesis, and cyclooxygenase activity in the skeletal muscles, while it was dependent on a complete substrate composition of the oral diet. Our results support the hypothesis that amino acids, probably in concerted action with locally produced tissue IGF-I, stimulate protein synthesis in skeletal muscles during refeeding.
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PMID:The role of diet components, gastrointestinal factors, and muscle innervation on activation of protein synthesis in skeletal muscles following oral refeeding. 1031 56

A 33 year old woman was investigated for an atypical case of Cushing's syndrome with suppressed early morning plasma cortisols. Chronic hypercortisolism was confirmed by classical biological criteria (24 h urinary cortisol excretion, dexamethasone suppression tests); more detailed dynamic and pharmacological tests revealed unanticipated features: spontaneous circadian plasma cortisol variations showed post prandial peaks; they could be induced by oral--but not intravenous--glucose tolerance tests, and were inhibited by the concomitant administration of Sandostatin (a somatostatin analog). Adrenal CT scan identified a 2 cm unilateral adenoma with ipsilateral and contralateral atrophy. Surgical removal of the tumor cured the hypercortisolism with hypocortisolism. Comparative analysis of the tumoral and normal tissues showed that only the former responded in vitro to GIP (Gastric Inhibitory Polypeptide) and contained the specific mRNA of the GIP receptor. This case illustrates a new pathophysiological mechanism of tumorigenesis due to the aberrant expression of a seven transmembrane domain receptor in a tumoral tissue. The nature of the given receptor induced a particular clinical phenotype related to food intake.
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PMID:[Aberrant expression of the GIP (Gastric Inhibitory Polypeptide) receptor in an adrenal cortical adenoma responsible for a case of food-dependent Cushing's syndrome]. 1033 44


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