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)

Enterocutaneous fistulas (ECFs) are a complex topic in terms of classification. ECF-related morbidity and mortality can be high due to fluid loss and electrolyte imbalance, sepsis, and malnutrition. Most prognostic factors influencing the outcome of ECF are now well-known. ECF treatment is complex; and, based on various situations, it can be surgical or conservative/ medical. Depending on fistula site and nutritional status, clinicians have to decide whether total parenteral or enteral nutrition should be established. In cases where total parenteral nutrition alone for 7 days has failed to influence the high output fistulas, overall data support the use of adjuvant drug, somatostatin, or its synthetic analogue, octreotide. Somatostatin 250 microg/d and octreotide 300-600 microg/d have been tried along with total parenteral nutrition to decrease the healing time of ECFs and to reduce the number of complications.
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PMID:Nutrition and enterocutaneous fistulas. 1103 97

In the human, intrauterine growth retardation (IUGR) can result in persistent postnatal growth failure, which may be attributable, in part, to abnormal GH secretion. Whether putative alterations in GH secretion are the result of abnormalities intrinsic to the pituitary or reflect changes in the production of GH-releasing hormone or somatostatin (SS) is unknown. We tested the hypothesis that growth failure associated with IUGR or early postnatal food restriction (FR) is caused by a central defect in hypothalamic SS gene expression. Both models displayed persistent growth failure postnatally without any catch-up growth. We measured levels of SS mRNA levels in rats experimentally subjected to IUGR or FR. SS mRNA levels were measured by semiquantitative in situ hybridization throughout development. Levels of SS mRNA in the periventricular nucleus were significantly higher in both male and female IUGR rats in the juvenile and adult stages compared with matched controls (p < or = 0.05). FR was associated with higher SS mRNA levels only in neonatal female rats (p < or = 0.05). These results suggest that intrauterine malnutrition induces a persistent increase in the expression of SS mRNA in the periventricular nucleus, whereas early postnatal FR results in only a transient increase in SS gene expression. Because IGF-I levels were normal in juvenile IUGR and FR rats, central dysregulation of SS neurons does not appear to be the cause of early postnatal growth failure in either model. However, these observations are consistent with the hypothesis that nutritional stress at critical times during development can have persistent and potentially irreversible effects on organ function.
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PMID:Effects of intrauterine and early postnatal growth restriction on hypothalamic somatostatin gene expression in the rat. 1110 52

A reduction in the availability of oxygen and nutrients across the placenta in the last trimester of pregnancy may lead to intrauterine growth retardation (IUGR) which, in turn, may cause a persistent postnatal growth failure. However, it is unknown whether this persistent growth retardation is centrally mediated through alterations in the components of the growth hormone (GH)-axis. We tested the hypothesis that alterations in the development of the central components of the GH-axis contribute to the persistent growth failure observed after experimentally induced IUGR or early postnatal food restriction (FR) in the rat. Using semi-quantitative in situ hybridization, we compared somatostatin (SS), GH-releasing hormone (GHRH) and neuropeptide Y (NPY) mRNA levels in adult rats experimentally subjected to IUGR or FR. We report that IUGR increased the expression of SS mRNA in the periventricular nucleus (PeN) of adult male and female rats by 128% and 153% respectively, did not alter the expression of GHRH mRNA in the arcuate nucleus (ARC) and decreased the NPY mRNA expression in the ARC by 73% in males and 61% in females, whereas in the FR group no changes in the expression of these mRNAs were observed. These data show that the timing of malnutrition or the presence of the placenta is important for the long-term alterations since the effects only occurred in the prenatally induced growth retardation and not in the early postnatally induced growth retardation group.
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PMID:Persistent changes in somatostatin and neuropeptide Y mRNA levels but not in growth hormone-releasing hormone mRNA levels in adult rats after intrauterine growth retardation. 1118 65

Intrauterine growth retardation (IUGR) is associated with persistent postnatal growth retardation accompanied by dysfunction of the hypothalamic components of the growth hormone (GH) axis. At the adult stage, this is reflected by increased somatostatin (SS) and decreased neuropeptide Y (NPY) mRNA levels, whereas the GH-releasing hormone (GHRH) mRNA levels are normal and the output of GH remains unchanged. To extend our insight into the hypothalamic control of GH secretion in growth retarded rats, we determined galanin (GAL) mRNA levels at the adult stage of perinatally malnourished (i.e. IUGR and early postnatally food restricted) rats. Analyses included comparison of GAL mRNA levels in GHRH neurons in perinatally malnourished adult rats using a semi-quantitative double labeling in situ hybridization technique. We report that IUGR is accompanied by a 60% decrease in GAL mRNA levels in all GHRH neurons in the male IUGR group whereas a tendency towards a decrease was observed in the male early postnatally food restricted (FR) group. These effects became more pronounced when the analysis was restricted to GHRH neurons coexpressing GAL mRNA i.e. decreased GAL mRNA levels were seen in both male and female IUGR rats and in FR males. These data show that GAL mRNA levels in GHRH neurons are persistently decreased after perinatal malnutrition. Taking these results together with our previous data on SS, NPY and GHRH mRNA levels, we can conclude that IUGR leads to a reprogramming of the hypothalamic regulation of GH secretion.
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PMID:Decreased galanin mRNA levels in growth hormone-releasing hormone neurons after perinatally induced growth retardation. 1152 32

Postoperative enterocutaneous fistulas are usually the result of an anastomotic leak. The likelihood of a postoperative fistula developing depends on concomitant diseases. An established gastrointestinal fistula is associated with considerable morbidity and mortality. Appreciable losses of fluid, protein and electrolytes often result in malnutrition, which has a negative impact on wound infection and the mental performance of the patient. Conservative treatment must aim to compensate these deficits as early as possible. Adequate amounts of energy (carbohydrates and fats) vitamins and trace elements must be ensured by replacement measures. In addition to appropriate drainage of the intra-abdominal focus and the use of antibiotics, treatment with octreotide (somatostatin analogues) may be considered. For conservative treatment, however, free intestinal transit distal to the fistula must be ensured. If an enterocutaneous fistula fails to heal within two or three months under conservative treatment, surgical management must be applied.
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PMID:[Postoperative fistulas. How to close them]. 1253 59

Resection of the small bowel can lead to malabsorption of fluid, electrolytes, minerals, and other essential nutrients, resulting in malnutrition and dehydration. Individualized and tailored nutritional management for patients with short bowel syndrome (SBS) helps to optimize intestinal absorption, leading to nutritional independence such that a patient can resume as normal a lifestyle as possible. Parenteral nutrition (PN), used to supply the required nutrients following resection, is associated with a number of complications affecting patient morbidity and mortality. Attempts should be made to wean patients from PN to an oral diet as soon as possible. Dietary management is complex and needs to be individualized for each patient on the basis of his or her specific gastrointestinal anatomy, underlying disease, and lifestyle. In addition to nutrient intake, management of SBS also requires appropriate oral rehydration, vitamin and mineral supplementation, and pharmacotherapy. Several medications provide a useful adjunctive function to dietary intervention, including antidiarrheal agents, H2 antagonists and proton pump inhibitors, pancreatic enzymes, somatostatin analogs, antimicrobials, and trophic factors.
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PMID:Dietary and medical management of short bowel syndrome in adult patients. 1677 Jan 67

Ghrelin is produced by A-like cells (ghrelin cells) in the mucosa of the acid-producing part of the stomach. The mobilization of ghrelin is stimulated by nutritional deficiency and suppressed by nutritional abundance. In an attempt to identify neurotransmitters and regulatory peptides that may contribute to the physiological, nutrient-related regulation of ghrelin secretion, we challenged the ghrelin cells in situ with a wide variety of candidate messengers, including known neurotransmitters (e.g. acetylcholine, catecholamines), candidate neurotransmitters (e.g. neuropeptides), local tissue hormones (e.g. serotonin, histamine, bradykinin, endothelin), circulating gut hormones (e.g. gastrin, CCK, GIP, neurotensin, PYY, secretin) and other circulating hormones/regulatory peptides (e.g. calcitonin, glucagon, insulin, PTH). Microdialysis probes were placed in the submucosa of the acid-producing part of the rat stomach. Three days later, the putative messenger compounds were administered via the microdialysis probe (reverse microdialysis) at a screening dose of 0.1 mmol l(-1) for regulatory peptides and 0.1 and 1 mmol l(-1) for amines and amino acids. The rats were awake during the experiments. The resulting microdialysate ghrelin concentration was monitored continuously for 3 h (radioimmunoassay), thereby revealing stimulators or inhibitors of ghrelin secretion. Dose-response curves were constructed for each candidate messenger that significantly (p<0.05) affected ghrelin mobilization at the screening dose. Peptides that showed a (non-significant) tendency to affect ghrelin release at the screening dose were also given at a dose of 0.3 or 1 mmol l(-1). Adrenaline, noradrenaline, endothelin and secretin stimulated ghrelin release, while somatostatin and GRP inhibited. Whether these agents act directly or indirectly on the ghrelin cells remains to be investigated. All other candidate messengers were without measurable effects, including acetylcholine, serotonin, histamine, GABA, aspartic acid, glutamic acid, glycine, VIP, PACAP, CGRP, substance P, NPY, PYY, PP, gastrin, CCK, GIP, insulin, glucagon, GLP and glucose.
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PMID:Secretion of ghrelin from rat stomach ghrelin cells in response to local microinfusion of candidate messenger compounds: a microdialysis study. 1757 35

Patients with anorexia nervosa (AN) may develop multiple endocrine abnormalities, including amenorrhea, hyperactivity of the hypothalamus-pituitary-adrenal axis, hypothyroidism and particular changes in the activity of the growth hormone (GH)/insulin-like growth factor I (IGF-I) axis. Exaggerated GH secretion and reduced IGF-I levels are usually found in AN, as well as in conditions of malnutrition and malabsorption, insulin-dependent diabetes mellitus, liver cirrhosis and catabolic states. In AN, GH hypersecretion at least partially reflects malnutrition-induced peripheral GH resistance, which leads to reduced IGF-I synthesis and release; this implies an impairment of the negative IGF-I feedback action on GH secretion. On the other hand, primary alterations in the neural control of GH secretion cannot be ruled out. The neuroendocrine alterations include enhanced somatotroph responsiveness to growth hormone releasing hormone (GHRH) and impaired GH response to most central nervous system-mediated stimuli. Particular resistance to cholinergic manipulation has also been demonstrated, thus suggesting a somewhat specific alteration in the somatostatin (SS)-mediated cholinergic influence on GH secretion. Moreover, paradoxical GH responses to glucose load, thyrotropin releasing hormone (TRH) and luteinizing hormone releasing hormone (LHRH) have also been reported. The effect of reduced leptin levels on GH hypersecretion in AN is still unclear, but ghrelin (the gastric hormone that is a natural ligand of the GH secretagogue receptor and strongly stimulates somatotroph secretion) is thought to play a major role. Regardless of the supposed central and peripheral alterations, it has to be emphasised that the activity of the GH/IGF-I axis in AN is generally restored by nutritional and stable weight gain. It therefore reflects an impaired nutritional state and cannot be considered a primary hallmark of the disease.
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PMID:GH/IGF-I axis in anorexia nervosa. 1764 63

Chylothorax is the accumulation of chyle in the pleural space, as a result of damage to the thoracic duct. Chyle is milky fluid enriched with fat secreted from the intestinal cells and lymphatic fluid. Chylothorax in children, is most commonly seen as a complication of cardiothoracic surgery but may occur in newborns or conditions associated with abnormal lymphatics. The diagnosis is based on biochemical analysis of the pleural fluid, which contains chylomicrons, high levels of triglycerides and lymphocytes. Investigations to outline the lymphatic channels can prove helpful in some cases. Initial treatment consists of drainage, dietary modifications, total parenteral nutrition and time for the thoracic duct to heal. Somatostatin and its analogue octreotide may be useful in some cases. Surgery should be considered for patients who fail these initial steps, or in whom complications such as electrolyte and fluid imbalance, malnutrition or immunodeficiency persist. Surgical intervention may be attempted thoracoscopically with repair or ligation of the thoracic duct.
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PMID:Chylothorax: diagnosis and management in children. 1987 10

Chylous ascites as a result of laparoscopic donor nephrectomy (LDN) is a rare complication that carries significant morbidity, including severe protein-calorie malnutrition and an associated immunocompromised state. We report a patient who underwent hand-assisted left LDN and subsequently developed chylous ascites. He failed conservative therapy including low-fat diet with medium-chain triglycerides (LFD/MCT) and oral protein supplementation as well as strict NPO status with intravenous (IV) total parenteral nutrition (TPN) and subcutaneous (SQ) somatostatin analogue administration. Laparoscopic re-exploration and intracorporeal suture ligation and clipping of leaking lymph channels successfully sealed the chyle leak. We review the literature to date including diagnosis, incidence, management options, psychosocial aspects and clinical outcomes of chylous ascites after LDN.
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PMID:Chylous ascites requiring surgical intervention after donor nephrectomy: case series and single center experience. 1995 36


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