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

A 63-year-old Japanese man complained of hematuria and pollakisuria for several months. Computed tomography and cystography disclosed an infiltrative tumor mass in the irregularly thickened apical and posterior walls of the urinary bladder. Narrowing of the vesical lumen and posterior extension of the tumor into the pelvic cavity were also noted. After palliative ureterocutaneostomy, 60 Gy irradiation was given locally. The patient died of cachexia seven months later. Autopsy revealed neuroendocrine carcinoma of the urinary bladder with extensive invasions and metastases to the pelvic and peritoneal cavities, liver, lungs, vertebrae, left kidney and retroperitoneal lymph nodes. Histologically, atypical tumor cells with eosinophilic cytoplasm formed solid nests and anastomosing cords with pseudoglandular structures. No other histologic tumor components were included. An intact urachal remnant was found at the vesical apex while features of metaplastic cystitis were absent. In addition to positive carcinoembryonic antigen and cytokeratin, the argyrophilic cancer cells were immunoreactive for neuron-specific enolase, chromogranin A, serotonin, neuropeptide Y, glicentin, somatostatin, neurotensin and calcitonin. Ultrastructurally, neurosecretory-type granules, with a mean diameter of 166 nm, were identified in the cytoplasm of the tumor cells. To discuss the histogenesis of the tumor, 44 previously reported cases of neuroendocrine carcinoma of the urinary bladder were reviewed.
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PMID:Neuroendocrine carcinoma of the urinary bladder: case report and review of the literature. 194 51

High circulating levels of somatostatin (SRIF) were detected in a patient with a metastatic tumour after development of diabetic ketoacidosis (DKA). Fasting insulin and C-peptide levels were markedly suppressed, but plasma glucagon was not suppressed below normal. Progressive cachexia ensued; at autopsy a poorly differentiated non-small cell neuroendocrine carcinoma metastatic to liver was found. Small gallstones were noted. Electron microscopy of tumour tissue showed neurosecretory granules and tonofilament bundles. Immunohistochemical staining of tumour cells was diffusely positive for carcinoembryonic antigen, bombesin-like immunoreactivity, and calcitonin with focal immunoreactivity for SRIF, serotonin, neuron-specific enolase, chromogranin, and epithelial membrane antigen. Column chromatography of plasma and tumour extract revealed five or more peaks of material with SRIF-like immunoreactivity (SRIF-LI): predominantly SRIF-28 and intermediates in tumour extract, and SRIF-14 and an intermediate between SRIF-28 and SRIF-14 in plasma, DKA in this case of somatostatinoma syndrome may reflect differential effects of tumour production of larger molecular weight SRIF forms on insulin and glucagon secretion.
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PMID:Malignant somatostatinoma presenting with diabetic ketoacidosis. 282 97

Leptin is a hormone secreted by the adipocytes that regulates food intake and energy expenditure. It is known that growth hormone (GH) secretion is markedly influenced by body weight, being suppressed in obesity and cachexia, and recent data have demonstrated that GH release is regulated by leptin levels. Although one of the sites of action of leptin is likely to be the hypothalamus, since leptin receptor mRNA is particularly abundant in several hypothalamic nuclei, the mechanisms by which leptin regulates GH secretion are not yet known. The aim of the present study was to investigate whether leptin could act at the hypothalamic level modulating somatostatin and GH-releasing hormone (GHRH) expression. The administration of anti-GHRH serum (500 microl, i.v.) completely blocked leptin-induced GH release in fasting rats. In contrast, the treatment with anti-somatostatin serum (500 microl, i.v.) significantly increased GH release in this condition. Furthermore, leptin administration (10 microg, i.c.v.) to intact fasting animals reversed the inhibitory effect produced by fasting on GHRH mRNA levels in the arcuate nucleus of the hypothalamus, and increased somatostatin mRNA content in the periventricular nucleus. Finally, leptin administration (10 microgram, i.c.v.) to hypophysectomized fasting rats increased GHRH mRNA levels, and decreased somatostatin mRNA content, indicating an effect of leptin on hypothalamic GHRH- and somatostatin-producing neurons. These findings suggest a role for GHRH and somatostatin as mediators of leptin-induced GH secretion.
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PMID:Role of growth hormone (GH)-releasing hormone and somatostatin on leptin-induced GH secretion. 989 45

Spontaneous amyloidosis occurs in many nonhuman primate species but remains difficult to diagnose and treat. Nonhuman primates continue to offer promise as animal models in which to study amyloidosis in humans. Amyloidosis was not diagnosed clinically but was found histologically in four male and 36 female baboons. The baboons averaged 18 years of age at death (range, 7-28 years). Clinical signs, if present, were hyperglycemia and cachexia. Blood glucose values were elevated in 12 of 30 baboons with available clinical pathology data. Four baboons had been clinically diagnosed as diabetic and three were treated with insulin. Amyloid was found in the islets of Langerhans of the pancreas in 40 baboons; 35 baboons had amyloid only in the islets of Langerhans. Amyloid was found in nonislet tissue of baboons as follows: five, nonislet pancreas; four, intestine and adrenal; three, kidney; two, prostate and spleen; and one each, lymph node, liver, gall bladder, stomach, tongue, urinary bladder, and salivary gland. Sections of paraffin-embedded tissues were evaluated for amyloid with hematoxylin and eosin (HE) and congo red (CR) staining, and using immunohistochemistry for human islet amyloid polypeptide (IAPP), calcitonin gene-related peptide (CGRP), glucagon, pancreatic polypeptide (PP), somatostatin (SS), and porcine insulin. Islet amyloid was positive with HE in 40 baboons, with CR in 39 baboons, and with IAPP and CGRP in 35 baboons. IAPP and CGRP only stained islet amyloid. PP, SS, glucagon, and porcine insulin did not stain amyloid. Islet amyloidosis in the baboon appears to be difficult to diagnose clinically, age-related, and similar to islet amyloidosis in other species. The baboon may be a good model for the study of islet amyloidosis in humans.
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PMID:Spontaneous pancreatic islet amyloidosis in 40 baboons. 1211 51

Chylous effusions have an identical appearance to milk and occur when the thoracic duct is blocked. Since chyle represents direct absorption of fat from the small intestine lacteals, it is rich in fat, calories, vitamins and immunoglobulins. Drainage of this milk-like fluid from any cavity (chest or abdomen) results in rapid weight loss and profound cachexia. The recognition of this milk-like fluid as chyle is urgent for the implementation of the correct treatment. In adults, lymphoma is one of the commonest malignancies to cause blockages in the thoracic duct. Once the diagnosis is made, conservative treatment with strict dietary adjustment often fails to prevent weight loss or resolve the underlying cause. Since the condition is uncommon, no guidelines exist. Many surgeons recommend early surgical intervention before the patient becomes too weak. Surgery may also fail. We report the case of a 62-year-old man with chylous effusions and a weight loss of 30 kg. The nature of the effusion was unrecognized for the first 16 weeks. Upon diagnosis, dietary adjustment was made and a lymphangiogram organized with a view to surgery. Literature searches revealed two cases in which somatostatin was used after surgical procedures failed. We therefore used octreotide (a synthetic analogue of somatostatin). We report complete resolution of the condition within 72 h leading to the resumption of a normal diet and discharge within 2 weeks.
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PMID:Chylous effusions complicating lymphoma: a serious event with octreotide as a treatment option. 1280 12

Ghrelin is a 28-amino-acid peptide predominantly produced by the stomach, while substantially lower amounts derive from other tissues including the pancreas. It is a natural ligand of the GH secretagogue (GHS) receptor (GHS-R1a) and strongly stimulates GH secretion, but acylation in serine 3 is needed for its activity. Ghrelin also possesses other endocrine and nonendocrine actions reflecting central and peripheral GHS-R distribution including the pancreas. The wide spectrum of ghrelin activities includes orexigenic effect, control of energy expenditure, and peripheral gastroenteropancreatic actions. Circulating ghrelin levels mostly reflect gastric secretion as indicated by evidence that they are reduced by 80% after gastrectomy and even after gastric by-pass surgery. Ghrelin secretion is increased in anorexia and cachexia but reduced in obesity, a notable exception being Prader-Willi syndrome. The negative association between ghrelin secretion and body weight is emphasized by evidence that weight increase and decrease reduces and augments circulating ghrelin levels in anorexia and obesity, respectively, and agrees with the clear negative association between ghrelin and insulin levels. In fact, ghrelin secretion is increased by fasting whereas it is decreased by glucose load as well as during euglycemic clamp but not after arginine or free fatty acid load in normal subjects; in physiological conditions, however, the most remarkable inhibitory input on ghrelin secretion is represented by somatostatin as well as by its natural analog cortistatin that concomitantly reduce beta-cell secretion. This evidence indicates that the endocrine pancreas plays a role in directly or indirectly modulating ghrelin secretion.
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PMID:Ghrelin and the endocrine pancreas. 1461 Feb 95

Chylous effusions in adults are commonly associated with malignant disease. Although the condition is rare, their occurrence presents a significant management problem. A review of the literature demonstrates the high mortality of this condition in the past from cachexia and infection or after surgical attempts at correction. The first report of somatostatin use in chylous effusions was a decade ago. Since 2000, case reports of successful treatment in infants and neonates with intravenous somatostatin or octreotide have been published. For adults, few reports exist. We describe a case series of seven patients, all with malignancy. In each case, there was a systematic approach to treatment using subcutaneous octreotide and a fat-free diet, resulting in complete resolution of the condition. Although no guidelines are available for the management of chylous effusions, our non-invasive approach avoided lymphangiogram, surgery and allowed early discharge.
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PMID:The successful treatment of chylous effusions in malignant disease with octreotide. 1583 May 74

Retroperitoneal chylous effusion after urological surgery is a rare and serious complication. Failure in treatment may result in cachexia, threatening the life of the patient. We present the treatment of two cases of postoperative chyloretroperitoneum with the use of somatostatin, octreotide and total parenteral nutrition. In Case 1, an 87-year-old man, a retroperitoneal lymphatic fistula occurred four days after the resection of the left kidney due to carcinoma, whereas in Case 2, a 56-year-old man, a continuous lymph fistula from the renal fossa occurred one month after resection of the right adrenal pheochromocytoma. Case 1 was treated with intravenous administration of somatostatin, and in Case 2, treatment consisted of subcutaneous administration of octreotide, in combination with total parenteral nutrition and other symptomatic therapies. In both cases, lymph exudation was terminated in about two weeks, and the patients recovered. Somatostatin therapy and total parenteral nutrition can effectively treat chyloretroperitoneum.
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PMID:Management of postoperative chyloretroperitoneum in adults. 1978 66

Somatostatin has been shown to have direct antiproliferative activity against various animal and human tumors and may be useful for long-term treatment of cancer patients. However, the metabolic effects of long-term somatostatin therapy have not been studied in the tumor-bearing host. It is known that somatostatin inhibits growth hormone and insulin secretion, and has inhibitory functions at all levels of the gastrointestinal tract. These properties may be especially detrimental to the tumor-bearing host which already suffers the cachectic effect of malignancy. This study examined the effect of the long-term somatostatin analogue octreotide (SMS) on host and tumor tissues in rats bearing a mammary adenocarcinoma (MAC-33). In vitro studies demonstrate that SMS (10-1000 ng/ml) has no direct effect on tumor cell proliferation in this model. Thirty female tumor-bearing Lewis rats were randomized to two groups. The treatment group received 175 mu g/kg SMS injections ip twice daily for 25 days; the placebo group received saline injections by the same route and schedule. Biochemical studies revealed a significant increase in tumor and liver protein/DNA ratio and decreased skeletal muscle protein/DNA content as a result of SMS treatment. These alterations in tumor and muscle composition are indicative of tumor growth and host catabolism. Biologic parameters demonstrated no significant change in carcass weight, tumor weight, or tumor metastasis from SMS treatment. Thus, a discordance is found between gross biologic parameters (indicating no significant effect of SMS) and more subtle biochemical indices (indicating progressive tumor growth and muscle protein catabolism). SMS therapy may produce adverse biochemical effects on host muscle which simulate cachexia when used chronically in the tumor-bearing host.
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PMID:Biochemical and biologic effects of somatostatin therapy on tumor-growth and host metabolism. 2155 35

Nuroendocrine neoplasms (NENs) are a group of rare neoplasms originating from dispersed neuroendocrine cells, mainly of the digestive and respiratory tract, showing characteristic histology and immunoprofile contributing to classification of NENs. Some NENs have the ability to produce biogenic amines and peptide hormones, which may be associated with clinical syndromes like, e.g., the carcinoid syndrome caused by unmetabolized overproduced serotonin, hypoglycemic syndrome in case of insulinoma, or Zollinger-Ellison syndrome accompanying gastrinoma. Diagnostics for these include ultrasound with endoscopic ultrasound (EUS), computed tomography (CT), magnetic resonance imaging (MRI), and positron-emission tomography/computed tomography (PET/CT). Different nuclear medicine procedures can also be used, like somatostatin analogues scintigraphy (SRS) and 68Ga-Dota-Peptide PET/CT, as well as biochemical methods to determine the level of general neuroendocrine markers, such as chromogranin A (CgA), 5-hydroxyindolacetic acid (5-HIAA), synaptopfysin and cell type-specific peptide hormones, and neurotransmitters like gastrin, insulin, serotonin, and histamine. NENs influence the whole organism by modulating metabolism. The treatment options for neuroendocrine neoplasms include surgery, somatostatin analogue therapy, radionuclide therapy, chemotherapy, molecular targeted therapies, alpha-interferon therapy, and inhibitors of serotonin production. In the case of hypersensitivity to biogenic amines, a diet that limits the main sources of amines should be used. The symptoms are usually connected with histamine, tyramine and putrescine. Exogenic sources of histamine are products that take a long time to mature and ferment. Patients with a genetic insufficiency of the diamine oxidase enzyme (DAO), and those that take medicine belonging to the group of monoamine oxidases (MAO), are particularly susceptible to the negative effects of amines. Diet plays an important role in the initiation, promotion, and progression of cancers. As a result of the illness, the consumption of some nutrients can be reduced, leading to nutritional deficiencies and resulting in malnutrition. Changes in metabolism may lead to cachexia in some patients suffering from NENs. The aim of this narrative review was to advance the knowledge in this area, and to determine possibilities related to dietary support. The authors also paid attention to role of biogenic amines in the treatment of patients with NENs. We can use this information to better understand nutritional issues faced by patients with gastroenteropancreatic neuroendocrine neoplasms (GEP-NENs), and to help inform the development of screening tools and clinical practice guidelines.
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PMID:The Neuroendocrine Neoplasms of the Digestive Tract: Diagnosis, Treatment and Nutrition. 3242 94


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