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)

Hyperglycemia, dyslipidemia, and associated insulin resistance are hallmarks of diabetes mellitus. Purposes of the study reported here were to develop practical methods for assessment of in vivo insulin sensitivity and determine contributions of hyperglycemia and dyslipidemia to insulin resistance in the porcine model of alloxan-induced diabetes mellitus and dyslipidemia. Male Yucatan swine groups were treated for 20 weeks: control (C), high fat-fed (2% cholesterol) hyperlipidemic (H), alloxan-induced diabetic normolipidemic (D), diabetic high fat-fed (diabetic dyslipidemic, DD), and diabetic dyslipidemic treated with the lipid-lowering agent atorvastatin (DDA). Plasma cholesterol concentration increased sixfold in animals of groups H, DD, and DDA, whereas triglyceride concentration increased threefold in animals of group DD only. Diabetics had decreases in glucose tolerance and pancreatic immunostaining for insulin. Use of the gold standard hyperinsulinemic euglycemic clamp procedure indicated that maximal insulin-stimulated glucose uptake was similar to that in humans, but this method was not practical for use in pigs. Instead, a more convenient and valid insulin sensitivity test involving suppression of insulin secretion with somatostatin and a single insulin injection was used. Insulin sensitivity was greatly impaired by anesthesia with isoflurane, but was not affected by use of the anxiolytic agent diazepam. Insulin sensitivity decreased by 75% in diabetics (groups D, DD, DDA), compared with animals of groups C and H, and was inversely related to fasting blood glucose concentration (r = -0.72). Insulin treatment to restore blood glucose values of diabetics (> 250 mg/dl) to near control values (< 100 mg/dl) promptly restored insulin sensitivity to control values. We conclude that hyperglycemia is a major cause of insulin resistance in the porcine model of alloxan-induced diabetes mellitus and dyslipidemia.
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PMID:Hyperglycemia-induced insulin resistance in diabetic dyslipidemic Yucatan swine. 1262 7

Acutely increased intra-abdominal pressure (IAP) may lead to abdominal compartment syndrome (ACS), which ischaemia/reperfusion (I/R) injury plays an important role. The main goal of the management of ACS is to lower the intra-abdominal pressure despite reperfusion injury. Octreotide (OCT), a synthetic somatostatin analogue, lowers the splanchnic perfusion. The aim of this study was to investigate whether OCT improves the reperfusion injury after decompression of acute abdominal hypertension.Under anesthesia, a catheter was inserted intraperitoneally and using an aneroid manometer connected to the catheter, IAP was kept at 20 mmHg (ischemia group; I) for 1h. In the I/R group, pressure applied for an hour was decompressed and 1h reperfusion period was allowed. In another group of I/R, OCT was administered (50 microg/kg i.p.) immediately before the decompression of IAP. The results demonstrate that kidney and lung tissues of malondialdehyde (MDA; an end product of lipid peroxidation) levels and myeloperoxidase (MPO; index of tissue neutrophil infiltration) activity were elevated, while glutathione (GSH; a key to antioxidant) levels were reduced in I/R group (P<0.001). Moreover, OCT treatment applied in the I/R group reduced the elevations in blood urea nitrogen (BUN) and serum creatinine levels. Our results implicate that IAP causes oxidative organ damage and OCT, by reducing splanchnic perfusion and controlling the reperfusion of abdominal organs, could improve the reperfusion-induced oxidative damage. Therefore, its therapeutic role as a "reperfusion injury-limiting" agent must be further elucidated in IAP-induced abdominal organ injury.
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PMID:Octreotide: a new approach to the management of acute abdominal hypertension. 1470 53

Ischemia/reperfusion injury plays an important role in the pathogenesis of abdominal compartment syndrome, which is characterized by increased intra-abdominal pressure. The aim of this study was to investigate whether octreotide, a synthetic somatostatin analogue, improves the reperfusion injury after decompression of acute abdominal hypertension. This study was carried out in Wistar albino rats. With the rats under anesthesia, an arterial catheter was inserted intraperioneally and with the use of an aneroid manometer connected to the catheter, intra-abdominal pressure was kept at 20 mm Hg (ischemia group) for 1 hour. In the ischemia/reperfusion group, pressure applied for 1 hour was decompressed and a 1-hour reperfusion period was allowed. In another ischemia/reperfusion group, octreotide was administered (50 microg/kg intraperitoneally) immediately before the decompression of intra-abdominal pressure. At the end of the experiment, liver and intestinal tissues were taken and malondialdehyde (an index of lipid peroxidation) and glutathione (a key to antioxidant) levels and myeloperoxidase (an index of tissue neutrophil infiltration) activity were estimated. The results demonstrated that tissue levels of malondialdehyde and myeloperoxidase activity were elevated, whereas glutathione levels were reduced in both the ischemia and ischemia/reperfusion groups. Octreotide treatment reversed these oxidant responses. In conclusion, increased intra-abdominal pressure causes oxidative organ damage and octreotide, by controlling the reperfusion of abdominal organs and inhibiting neutrophil infiltration, could improve the reperfusion-induced oxidative damage. Therefore its therapeutic role as a "reperfusion injury-limiting" agent must be further elucidated in intra-aortic pressure-induced abdominal organ injury.
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PMID:Octreotide improves reperfusion-induced oxidative injury in acute abdominal hypertension in rats. 1474 43

This study presents the distribution and chemical coding of neurons in the porcine intramural ganglia of the urinary bladder trigone (IG-UBT) demonstrated using combined retrograde tracing and double-labelling immunohistochemistry. Retrograde fluorescent tracer Fast Blue (FB) was injected into the wall of both the left and right side of the bladder trigone during laparotomy performed under pentobarbital anaesthesia. Ten-microm-thick cryostat sections were processed for double-labelling immunofluorescence with antibodies against tyrosine hydroxylase (TH), dopamine beta-hydroxylase (DBH), neuropeptide Y (NPY), somatostatin (SOM), galanin (GAL), vasoactive intestinal polypeptide (VIP), nitric oxide synthase (NOS), calcitonin gene-related peptide (CGRP), substance P (SP), Leu5-enkephalin (LENK) and choline acetyltransferase (ChAT). IG-UBT neurons formed characteristic clusters (from a few to tens neuronal cells) found under visceral peritoneum or in the outer muscular layer. Immunohistochemistry revealed four main populations of IG-UBT neurons: SOM- (ca. 35%), SP- (ca. 32%), ChAT- and NPY- immunoreactive (-IR) (ca. 23%) as well as non-adrenergic non-cholinergic nerve cells (ca. 6%). This study has demonstrated a relatively large population of differently coded IG-UBT neurons, which constitute an important element of the complex neuro-endocrine system involved in the regulation of the porcine urogenital organ function.
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PMID:Distribution and chemical coding of neurons in intramural ganglia of the porcine urinary bladder trigone. 1504 94

Rapid opiate detoxification (ROD) is a technique whereby the opiate-dependent patient is withdrawn acutely, under anesthesia, from the opioid. Following detoxification, patients experience severe back pain and restlessness often accompanied by a restless-leg-syndrome. We evaluated gabapentin given immediately following detoxification to attenuate these symptoms. In addition, we evaluated the use of the somatosensory-evoked potential (SEP) as a parameter to quantitate pain responses. Patients (n=21; mean age 32.5 +/- 7 SD; 12 males, 9 females) underwent ROD with naltrexone (2 x 50 mg) during propofol anesthesia and artificial ventilation (IPPV). Sympathetic overshoot was attenuated by clonidine, and increased bowl movement was managed by continuous i.v. somatostatin. Back pain, restlessness, and restless-leg-syndrome were treated with gabapentin (1200 mg) in the ICU. Efficacy was assessed by the patient's subjective ratings of restlessness (0-4). In addition, measurements of amplitude (microV), latency (ms) of late N100-peak of the somatosensory evoked potential (SEP), and tolerance to an increased electrical nociceptive stimulus (mA) to the forearm were performed. Data were compared to pre-treatment control and to the period shortly after detoxification. From a mean of 8.4 +/- 2.5 microV, N100-peak increased to a mean of 12.3 microV +/- 3.3 (p < 0.005) following opioid detoxification. Gabapentin reduced amplitude height to a mean of 3.5 +/- 1.5 microV. Also, tolerance to nociceptive stimulus, which had dropped to 4.4 mA, increased to 12.5 mA (p < 0.01), while intensity for restlessness and thrashing of limbs dropped from 3.2 to 1.2 (p < 0.05). The sudden displacement of the opiate from its receptor site induced by naltrexone, resulted in a post inhibitory SEP overshoot with an increase in nociceptive afferent volleys, and a lowering in pain threshold. This was associated with back pain, limb thrashing and a restless-leg-syndrome, all of which could be attenuated by gabapentin. The amplitude of late N100-peak parameter appears to be a potential candidate to quantify the increase of nociception in such patients.
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PMID:Use of gabapentin for attenuation of symptoms following rapid opiate detoxification (ROD)--correlation with neurophysiological parameters--. 1513 May 54

Somatostatin, probably acting through somatostatin type 2 receptors (SSTR2), is the main inhibitor of gastric acid secretion. We characterized gastric acid secretion in SSTR2 knockout mice, and used preferential somatostatin receptor agonists to assess the relative role of SSTR1, 2, 3, 4, and 5 on gastric acid secretion. Basal gastric acid secretion and the secretory response to a meal were similar in conscious wild-type and knockout mice. However, under urethane anesthesia, which releases endogenous somatostatin, SSTR2 knockout mice had a basal secretion 11-15-fold higher than wild-type animals (micromol/10 min:1.40+/-0.09 vs. 0.10+/-0.01, p<0.05). Gastrin immunoneutralization or H(2) receptors blockade (cimetidine), but not cholinergic blockade (atropine), reduced the high basal secretion in SSTR2 knockout mice. In SSTR2 knockout mice, gastrin and histamine stimulated acid secretion with similar efficacy, while in wild-type mice histamine was more effective than gastrin. SSTR2 knockout mice showed also a hypersecretory response to pylorus ligation compared with wild-type animals. In wild-type mice, somatostatin-14, SMS 201-995, and the SSTR2-preferential agonist, DC 32-87, inhibited gastrin-stimulated acid secretion with an order of potency SMS 201-995>DC 32-87>somatostatin-14. Preferential agonists for the SSTR1, 3, 4, and 5 were devoid of any effect. None of the compounds tested affected the high basal secretion observed under urethane anesthesia in SSTR2 knockout mice. These results show that gastric antisecretory effects of peripheral somatostatin are mediated solely through SSTR2. In the absence of functional SSTR2 other somatostatin receptors do not compensate for the lack somatostatin-SSTR2-mediated inhibition. Basal acid secretion and the response to a meal are normal in conscious SSTR2 knockout mice, suggesting the presence of somatostatin-independent mechanisms that compensate for the lack of somatostatin-SSTR2-mediated inhibitory responses.
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PMID:Role of somatostatin receptors on gastric acid secretion in wild-type and somatostatin receptor type 2 knockout mice. 1559 10

KP-102 (D-alanyl-3-(2-naphthyl)-D-alanyl-L-alanyl-L-tryptophyl-D-phenylalanyl-L-lysinamide dihydrochloride, growth hormone-releasing peptide-2, GHRP-2, pralmorelin, CAS 158861-67-7), is a potent synthetic growth hormone (GH) secretagogue. In the present study, the pharmacological characteristics of the GH-releasing property of KP-102 were investigated by means of in vivo and in vitro experiments. In conscious rats, the GH-releasing activity of KP-102 was more potent than that of exogenously injected GH-releasing hormone (GHRH). Under pentobarbital anesthesia in which endogenous somatostatin secretion is known to be decreased, KP-102 and GHRH, both showed an almost equivalent GH-releasing potency, which was also similar to that of KP-102 in conscious rats. Besides, KP-102 showed GH-releasing activity in conscious dogs as well, while GHRH failed to increase serum GH levels in conscious dogs. These findings suggest that the GH-releasing activity of KP-102 was less sensitive to GH suppression by endogenous somatostatin as compared with that of GHRH. The GH-releasing activity of KP-102 was completely absent in hypophysectomized rats, but present in median eminence-lesioned rats in which secreted GH amounts were significantly less than those normal rats, indicating necessity of the median eminence (endogenous GHRH) to exert the full activity of KP-102 in GH stimulation. KP-102 directly stimulated GH secretion from cultured rat anterior pituitary cells, although the GH-releasing potency of KP-102 was significantly weaker than that of GHRH in vitro. In conscious rats, KP-102 stimulated the secretion of both adrenocorticotrophic hormone (ACTH) and corticosterone, but not of prolactin. Three weeks administration of KP-102 showed growth-accelerating effect, a slight increase of body weight and wet weight of some organs in both normal and monosodium glutamate (MSG)-treated rats. These results suggest that KP-102 showed specific GH-releasing activity apart from slight ACTH secretion, and that the GH-releasing activity was stable in comparison with that of exogenously injected GHRH.
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PMID:Pharmacological characteristics of KP-102 (GHRP-2), a potent growth hormone-releasing peptide. 1564 70

We have looked for the presence of beta-endorphin and somatostatin in normal and inflamed pulps. In 25 adult rats, under anesthesia, small openings were made into the pulp on the mesial surface of both first molars on one side. One week later all four first molars were removed, half were processed for immunohistochemistry using specific antibodies to beta-endorphin, somatostatin, and CD3, a marker for T lymphocytes. The pulps of the remainder were removed, solubilized, and subjected to enzyme-linked immunosorbent assay for somatostatin and beta-endorphin. Many cells that labeled for beta-endorphin and somatostatin in the injured pulps also stained for CD3. The levels of both beta-endorphin and somatostatin, were higher in the exposed than in the uninjured pulps (t test, p < 0.05). beta-endorphin and somatostatin are both produced in increased amounts in the dental pulp during inflammation attributable, at least in part, to the presence of T lymphocytes producing these substances.
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PMID:Local opioids in the inflamed dental pulp. 1655 2

Acromegaly reduces life expectancy and leads to 3-5-fold increase in mortality. The main causes are cardiovascular, pulmonary and enhanced prevalence of deaths from malignancy. Successful therapy ought to normalize GH, IGF-I secretion, remove the adenoma mass and its local pressure effects and preserve pituitary functions intact to improve systemic morbidity and normalize mortality. The primary therapy for most patients with acromegaly is still transsphenoidal adenomectomy. The authors present a 64-year-old woman with diagnosed GH-secreting pituitary macroadenoma suffering from severe coronary heart disease and diabetes mellitus. Somatostatin analogue therapy was ineffective in our patient. She was unfit for transsphenoidal adenomectomy. The patient was qualified for coronary artery bypass grafting after cardiological investigation. We have decided to carry out the bypass grafting and transsphenoidal adenomectomy during one anaesthesia. Both surgical procedures and postoperative time were uncomplicated. Our patient feels well and she is in outpatient follow-up.
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PMID:[Severe cardiovascular complications due to the pituitary adenoma with acromegaly. An interdisciplinary approach to the treatment. A case report]. 1696 59

This paper presents an overview of the evolution of pituitary surgery for acromegaly. It begins with the first case, attempted in 1893, through the initial transsphenoidal successes in 1907-1910, to the development of effective craniotomy approaches, and ultimately to the resurrection of the transsphenoidal approach in the 1970s and thereafter. Today, the minimally endoscopic transnasal endoscopic approach is fast becoming the norm. Indications for surgery include active acromegaly, visual loss and other forms of mass effect, pituitary tumor apoplexy, and failure of other therapies (medical, radiation). Contraindications include advanced age, debility or other medical conditions increasing the risk of general anaesthesia or surgery. Surgery for acromegaly has the advantage of immediate lowering of the growth hormone excess, with endocrine remission rates of 70% for microadenomas and 50% for macroadenomas. When surgery fails to obtain remission, a program of therapy is designed for the patient to include adjunctive medical therapy (dopamine agonists, somatostatin analogs, and growth hormone receptor antagonists), radiation therapy or radiosurgery (Gamma knife, Cyberknife, etc.).
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PMID:Surgery for acromegaly: evolution of the techniques and outcomes. 1822 47


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