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)

Pancreatic islet peptides, as well as other gastrointestinal hormones, have been implicated in both the pathogenesis of obesity and the etiology of associated metabolic derangements. This study evaluated the pancreatic islet and gastrointestinal (GI) hormone response to oral glucose in 20 morbidly obese (151% above ideal body weight) patients. Glucose intolerance, hyperinsulinism, and exaggerated gastric inhibitory polypeptide (GIP) release occurred following glucose ingestion. Significant release of PP occurred in 14 patients, while only six patients had release of somatostatin. No significant changes in plasma concentrations of glucagon occurred. Since GIP is insulinotropic in the presence of hyperglycemia, the hyperinsulinism of morbid obesity may be secondary to the abnormally high glucose-stimulated GIP levels in these patients. Failure of glucagon suppression in response to oral glucose many contribute to the hyperglycemia noted. Somatostatin and pancreatic polypeptide may be responsible for some of the metabolic derangements of morbid obesity.
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PMID:Pancreatic islet hormone response to oral glucose in morbidly obese patients. 286 Aug 76

Many of the features of the dumping syndrome may be manifestations of hypovolemia and mechanical distension of the gut, resulting from abnormal fluid secretion in the upper gastrointestinal tract. The object of the present study was to assess the effect of somatostatin, an inhibitor of upper gastrointestinal secretions, on the response to a dumping provocation test, using a double-blind, placebo-controlled method. Four patients were studied; two had undergone total gastrectomy for gastric carcinoma and two had undergone gastric bypass for morbid obesity. Each subject received, on two separate occasions, a challenge of 200 ml of 50% glucose administered orally after an overnight fast. Somatostatin in 150 mm of NaCl (250 micrograms bolus followed by 300 micrograms/hr infusion) was given intravenously during one dumping provocation test and placebo (150 mm of NaCl) during the other according to a Latin square design. When the subjects received the placebo there were significant increases in pulse rate and packed cell volume after oral glucose (p less than 0.05, paired t test), which did not occur when they received somatostatin. The glucose challenge also produced a more rapid increase in serum osmolality and blood glucose during administration of placebo than when somatostatin was given. Marked diarrhea developed in all placebo-treated subjects but in none when they received somatostatin; however, three of the subjects developed marked abdominal pain during dumping provocation tests when treated with somatostatin, which did not occur when placebo was given. Although somatostatin appears to suppress some of the objective responses to a dumping provocation test, it may not prove particularly useful in the treatment of dumping symptoms.
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PMID:The effect of somatostatin on dumping after gastric surgery: a preliminary report. 286 91

The mucosal concentrations of seven regulatory peptides and the density properties and integrity of their storage granules have been studied in mucosal biopsies from the human jejunum in eight gastrointestinal disease states and compared with normal controls. In diseases with associated mucosal inflammation (coeliac disease, Crohn's disease with jejunal involvement, postinfective tropical malabsorption, and common variable immunodeficiency) there was a selective increase in fragility of the gastric inhibitory polypeptide (GIP) and somatostatin storage granules. The gastrin, motilin, enteroglucagon, secretin, and vasoactive intestinal polypeptide granules had normal properties in these conditions. In diseases in which diarrhoea occurred in the absence of changes in jejunal mucosal histology (irritable bowel syndrome, pancreatic insufficiency, jejuno-ileal bypass for morbid obesity, and purgative abuse) there were no abnormalities of the storage granules. Increased mucosal concentrations of all peptides except vasoactive intestinal polypeptide (VIP) were found in coeliac disease and selective increases of VIP found in Crohn's disease, motilin in the irritable bowel syndrome and gastrin and GIP in pancreatic insufficiency. It is suggested that the storage granule abnormalities in the diseases with abnormal mucosal histology are secondary to the inflammatory changes.
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PMID:Gastrointestinal regulatory peptide storage granule abnormalities in jejunal mucosal diseases. 614 62

Obesity is associated with different disturbances in endocrine function. Both spontaneous growth hormone (GH) secretion and its response to several stimuli have shown to be reduced in obese patients. The GH responses to GH-releasing hormone and other challenges by pyridostigmine suggest that the reduction in GH secretion is related to an increased somatostatinergic tone. Other experiments point to a down-regulation of somatostatin receptors in the somatotroph cell. Ghrelin administration is followed by a massive GH release, but the possibility that ghrelin or GHRH deficiency are the cause of GH deficiency in obesity is unlikely. The increase in free fatty acids in obesity might be related to GH reduction, since acipimox administration is able to reverse GH secretion. In women, abdominal obesity is associated with hyperandrogenism and low sex hormone-binding globulin levels. Obese men have low testosterone and gonadotrophin concentrations, specially in cases of morbid obesity. An increase in hypothalamic-pituitary-adrenal axis activity and some resistance to dexamethasone suppression have been described in abdominal obesity. This effect may be due to neuroendocrine alterations related to a genetic origin. Adrenal hyperfunction may favour cardiovascular and metabolic complications. There are no disturbances in thyroid function. Sometimes a reduction in prolactin response to several stimuli has been reported. This effect may be due to hyperinsulinaemia or to disturbances in the dopaminergic tone.
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PMID:[Neuroendocrine disturbances in obesity]. 1538 10

Obesity is associated to significant disturbances in endocrine function. Hyper insulinemia and insulin resistance are the best known changes in obesity, but their mechanisms and clinical significance are not clearly established. Adipose tissue is considered to be a hormone-secreting endocrine organ; and increased leptin secretion from the adipocyte, a satiety signal, is a well-established endocrine change in obesity. In obesity there is a decreased GH secretion. Impairment of somatotropic function in obesity is functional and may be reversed in certain circumstances. The pathophysiological mechanism responsible for low GH secretion in obesity is probably multifactorial. There are many data suggesting that a chronic state of somatostatin hypersecretion results in inhibition of GH release. Increased FFA levels, as well as a deficient ghrelin secretion, probably contribute to the impaired GH secretion. In women, abdominal obesity is associated to hyperandrogenism and low sex hormone-binding globulin levels. Obese men, particularly those with morbid obesity, have decreased testosterone and gonadotropin levels. Obesity is associated to an increased cortisol production rate, which is compensated for by a higher cortisol clearance, resulting in plasma free cortisol levels that do not change when body weight increases. Ghrelin is the only known circulating orexigenic factor, and has been found to be decreased in obese people. In obesity there is also a trend to increased TSH and free T3 levels.
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PMID:[Endocrine function in obesity]. 2182 29

Bariatric surgical procedure are increasingly and successfully applied in the treatment of morbid obesity. Nevertheless, these procedures are not devoid of potential long-term complications. Dumping syndrome may occur after procedures involving at least partial gastric resection or bypass, including Roux-en-Y gastric bypass (RYGB) and sleeve gastrectomy. Diagnosis is based on clinical alertness and glucose tolerance testing. Treatment may involve dietary measures, acarbose and somatostatin analogues, or surgical reintervention for refractory cases. Gastro-esophageal reflux disease (GERD) can be aggravated by vertical banded gastroplasty and sleeve gastrectomy procedures, but pre-existing GERD may improve after RYGB and with adjustable gastric banding. Nutrient deficiencies constitute the most important long-term complications of bariatric interventions, as they may lead to haematological, metabolic and especially neurological disorders which are not always reversible. Malabsorptive procedures, poor postoperative nutrient intake, recurrent vomiting and poor compliance with vitamin supplement intake and regular follow-up are important risk factors. Preoperative nutritional assessment and rigourous postoperative follow-up plan with administration of multi-vitamin supplements and assessment of serum levels is recommended in all patients.
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PMID:Complications of bariatric surgery: dumping syndrome, reflux and vitamin deficiencies. 2519 87