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)

To assess the effect of sepsis on ketone body (KB) kinetics in humans, we measured in normal and septic subjects KB appearance rate (Ra) before (initial state) and during a rise of free fatty acids (FFA) level (intravenous infusion of a triglycerides emulsion). We studied normal subjects in postabsorptive state and septic patients when receiving an hypocaloric intravenous infusion of glucose and amino acids or 12 h after its interruption. When receiving glucose and amino acids infusion, septic patients had higher glucose and insulin levels than normal subjects, and despite lower FFA concentrations (255 +/- 44 vs. 480 +/- 51 mumol/l, P less than 0.05) comparable initial KB Ra (2.50 +/- 0.10 vs. 2.48 +/- 0.30 mumol.kg-1.min-1). Triglyceride infusion increased FFA to comparable values (septic 780 +/- 130, normal 730 +/- 45 mumol/l), but KB Ra rose in septic patients only to 3.7 +/- 1.1 instead of 7.7 +/- 1.1 mumol.kg-1.min-1 as in normal subjects (P less than 0.05). Somatostatin infusion decreased the hyperinsulinemia of septic patients but did not restore a normal ketogenesis. After interruption of nutriment infusion, septic patients had normal FFA levels and only mild hyperglycemia and hyperinsulinemia. Their initial KB Ra was not modified. However, their response of KB Ra (increase to 6.27 +/- 2.0 mumol.kg-1.min-1) to raised FFA levels (842 +/- 170 mumol/l) was comparable to the response of normal subjects. In conclusion, although septic patients receiving an hypocaloric parenteral nutrition had a depressed ketogenesis they were able to restore a normal ketogenic capacity after a short-time caloric deprivation. Glucose and/or insulin appears to have a major role in this modulation of hepatic ketogenesis.
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PMID:Regulation of ketone body flux in septic patients. 259 97

The current studies were designed to evaluate the role of plasma insulin and glucose as regulators of intestinal glucose transport in vivo. Initially, rats received either intravenous glucose infusion or intraperitoneal streptozotocin to induce sustained hyperglycemic hyperinsulinemia or hyperglycemic hypoinsulinemia. Net jejunal uptake rates of glucose were measured in vivo at several perfusate concentrations, and the kinetic constants, corrected for diffusion barrier resistance, were derived. Maximal velocity (Jmax) was increased 1.8-fold by hyperglycemic hyperinsulinemia and 2.6-fold by hyperglycemic hypoinsulinemia compared with controls, whereas Km and passive permeability of glucose were unchanged. The rate of L-proline uptake at saturation conditions was not increased by these experimental interventions. The corrected kinetic constants for jejunal glucose transport in streptozotocin diabetic rats kept normoglycemic and normoinsulinemic with insulin were similar to controls. Finally, induction of normoglycemic hyperinsulinemia by intravenous glucose-insulin infusion increased Jmax 1.8-fold, similar to hyperglycemic hyperinsulinemia, but induction of hyperglycemic normoinsulinemia by intravenous glucose-somatostatin infusion did not change Jmax. In conclusion, changes in plasma insulin but not glucose concentration cause a specific and reversible increase in Jmax of intestinal glucose transport. Hypoinsulinemia is a more potent signal than hyperinsulinemia. The membrane level, microvillus or basolateral, at which insulin induces an increased number of glucose transporters in intestinal epithelial cells remains to be defined.
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PMID:Insulin modulates rat intestinal glucose transport: effect of hypoinsulinemia and hyperinsulinemia. 265 75

A 7-year-old spayed female Cocker Spaniel was hospitalized with a history of chronic vomiting, anorexia, and weight loss. Laboratory abnormalities included leukocytosis, metabolic alkalosis, hypoglycemia, hypoproteinemia, and hyperinsulinemia. Gastroscopy and ultrasonography revealed multiple gastric masses and a possible pancreatic mass, respectively. Examination of tissues obtained at necropsy showed a pancreatic adenocarcinoma with hepatic metastasis, gastric hypertrophy, and multiple duodenal ulcers. Immunocytochemical staining of the neoplasia was positive for pancreatic polypeptide (PP) and insulin and negative for gastrin, calcitonin, adrenocorticotropic hormone (ACTH), serotonin, L-enkephalin, chromagranin, glucagon, and somatostatin. Subsequent serum gastrin and PP assays showed a fasting hypergastrinemia with a normal response of gastrin to provocative testing and extremely increased PP values. The high PP values may have resulted in the vomiting and gastrointestinal ulceration. A PP-secreting tumor has not previously been reported in the dog.
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PMID:Pancreatic polypeptide and insulin-secreting tumor in a dog with duodenal ulcers and hypertrophic gastritis. 267 25

The functional and morphologic characteristics of free-draining, pancreatic segmental autografts (FDPS) were studied in 8 beagle dogs that had survived longer than 4 yr. After pancreatectomy, animals received FDPS autografts of the left pancreatic limb, representing approximately one-third of the total pancreas with iliac vessel anastamoses. The grafted recipients were given pancreatic enzyme supplements (Viokase). After transplantation (tx), all 8 animals sustained fasting euglycemia with no evidence of microvascular complications. After 4 yr, IVGTT revealed K-values (%/min) that were not significantly different from age-matched controls (2.9 +/- 0.5 versus 3.7 +/- 0.6, P greater than 0.05). Mean fasting serum insulin levels were significantly greater in the tx animals (49 +/- 5 microU/ml versus 12.2 microU/ml, P less than 0.001), although the incremental response to i.v. glucose (0.5 g/kg) was less than in controls (P less than 0.05). Mean fasting plasma C-peptide levels (0.09 +/- 0.01 pmol/ml versus 0.21 +/- 0.5 pmol/ml) and peak C-peptide responses to i.v. glucose were both significantly less than in controls. Sequential pancreatic biopsies up to 2.5 yr post-tx showed atrophy of the exocrine pancreas with coalescence of islets and mild fibrosis that did not progress with time. Immunoperoxidase stains confirmed the presence of insulin, glucagon, and somatostatin within nests of islet cells. Four years after transplantation of FDPS autografts in pancreatectomized dogs, excellent function is retained. The consequences of peripheral hyperinsulinemia remain to be determined.
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PMID:Long-term follow-up of canine segmental pancreatic autografts. 285 44

The effects in vivo of physiologic increases in insulin and amino acids on myocardial amino acid balance were evaluated in conscious dogs. Arterial and coronary sinus concentrations of amino acids and coronary blood flow were measured during a 30-min basal and a 100-min experimental period employing three protocols: euglycemic insulin clamp (plasma insulin equaled 70 +/- 11 microU/ml, n = 6); euglycemic insulin clamp during amino acid infusion (plasma insulin equaled 89 +/- 12 microU/ml, n = 6); and suppression of insulin with somatostatin during amino acid infusion (plasma insulin equaled 15 +/- 4 microU/ml, n = 6). Basally, only leucine and isoleucine were removed significantly by myocardium (net branched chain amino acid [BCAA] uptake equaled 0.5 +/- 0.2 mumol/min), while glycine, alanine, and glutamine were released. Glutamine demonstrated the highest net myocardial production (1.6 +/- 0.2 mumol/min). No net exchange was seen for valine, phenylalanine, tyrosine, cysteine, methionine, glutamate, asparagine, serine, threonine, taurine, and aspartate. In group I, hyperinsulinemia caused a decline of all plasma amino acids except alanine; alanine balance switched from release to an uptake of 0.6 +/- 0.4 mumol/min (P less than 0.05), while the myocardial balance of other amino acids was unchanged. In group II, amino acid concentrations rose, and were accompanied by a marked rise in myocardial BCAA uptake (0.4 +/- 0.1-2.6 +/- 0.3 mumol/min, P less than 0.001). Uptake of alanine was again stimulated (0.9 +/- 0.3 mumol/min, P less than 0.01), while glutamine production was unchanged (1.3 +/- 0.4 vs. 1.6 +/- 0.3 mumol/min). In group III, there was a 4-5-fold increase in the plasma concentration of the infused amino acids, accompanied by marked stimulation in uptake of only BCAA (6.8 +/- 0.7 mumol/min). Myocardial glutamine production was unchanged (1.9 +/- 0.4-1.3 +/- 0.7 mumol/min). Within the three experimental groups there were highly significant linear correlations between myocardial uptake and arterial concentration of leucine, isoleucine, valine, and total BCAA (r = 0.98, 0.98, 0.92, and 0.97, respectively); P less than 0.001 for each). In vivo, BCAA are the principal amino acids taken up by the myocardium basally and during amino acid infusion. Plasma BCAA concentration and not insulin determines the rate of myocardial BCAA uptake. Insulin stimulates myocardial alanine uptake. Neither insulin nor amino acid infusion alters myocardial glutamine release.
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PMID:Regulation of myocardial amino acid balance in the conscious dog. 285

The release of somatostatin from the pancreas and stomach following the ingestion of a meal and its increase in the peripheral circulation elicits an attenuation of postprandial hormone secretion such as insulin, pancreatic polypeptide and gastrin and retards the rate at which nutrients enter the circulation. Reduced tissue somatostatin content and/or an attenuated somatostatin release is associated with hyperinsulinism and obesity in certain animal models. In the obese Zucker rat, however, tissue somatostatin levels are increased and therefore the present study was designed to determine the effect of synthetic somatostatin on basal and postprandial arterial insulin levels in obese and lean Zucker rats. Synthetic somatostatin was infused at doses of 0.25, 0.5, 1 and 5 ng/kg X min before and after the intragastric instillation of a liver extract/sucrose test meal. In the obese rats somatostatin at a dose of 5 ng/kg X min reduced basal plasma insulin levels significantly, whereas no effect of somatostatin was observed on basal insulin levels in the lean animals at all doses employed. The integrated postprandial insulin response was reduced during 0.25, 0.5, 1 and 5 ng/kg X min somatostatin in the obese animals, whereas only 0.5 ng/kg X min and higher doses had an inhibitory effect in the lean rats. The degree of inhibition in relation to the postprandial insulin response during saline infusions was 35-230% in the obese and 30-100% in the lean Zucker rats within the range of somatostatin infusions employed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased sensitivity to somatostatin in obese Zucker rats. 285 37

To assess the role of hepatic autoregulation in defense against hypoglycemia, we compared the effects of complete blockade of glucose counterregulation with those of blockade of only neurohumoral counterregulation during moderate (approximately 50 mg/dl) and severe (approximately 30 mg/dl) hypoglycemia induced by physiologic hyperinsulinemia during subcutaneous infusion of insulin in normal volunteers. Compared with observations in control experiments, neurohumoral counterregulatory blockade (somatostatin, propranolol, phentolamine, and metyrapone), during which identical moderate hypoglycemia was achieved using the glucose clamp technique, resulted in suppressed glucose production (0.62 +/- 0.08 vs. 1.56 +/- 0.07 mg/kg per min at 12 h, P less than 0.01) and augmented glucose utilization (2.17 +/- 0.18 vs. 1.57 +/- 0.07 mg/kg per min at 12 h, P less than 0.01). Complete blockade of counterregulation (neurohumoral blockade plus prevention of hypoglycemia) did not further enhance the suppressive effects of insulin on glucose production. However, when severe hypoglycemia was induced during neurohumoral counterregulatory blockade, glucose production was nearly two times greater (1.05 +/- 0.05 mg/kg per min at 9 h) than that observed during complete counterregulatory blockade (0.58 +/- 0.08 mg/kg per min at 9 h, P less than 0.01) and that observed during mere neurohumoral blockade with moderate hypoglycemia (0.59 +/- 0.06 mg/kg per min at 9 h, P less than 0.01). These results demonstrate that glucose counterregulation involves both neurohumoral and hepatic autoregulatory components: neurohumoral factors, which require only moderate hypoglycemia for their activation, augment glucose production and reduce glucose utilization; hepatic autoregulation requires severe hypoglycemia for its activation and may thus serve as an emergency system to protect the brain when other counterregulatory factors fail to prevent threatening hypoglycemia.
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PMID:Role of hepatic autoregulation in defense against hypoglycemia in humans. 286 Jan 28

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

Glucose disposal rates (Rd) during an insulin clamp study reflect both basal and insulin-stimulated Rd. To quantify the amount of glucose taken up in response to a known increase in insulin concentration, two consecutive studies were performed on 10 patients with mild to moderate NIDDM (mean fasting glucose = 146 mg/dl) and 10 normal subjects. Endogenous insulin secretion was inhibited by somatostatin and plasma glucose level maintained at 180 mg/dl for 5. Rd (mg/m2/min) was determined isotopically for 2.5 h at insulin concentrations approximately 6 microU/ml and during 2.5 h of physiologic hyperinsulinemia at approximately 60 microU/ml (total glucose disposal), with the increase in Rd resulting from the approximate 10-fold elevation of plasma insulin concentration defined as insulin-stimulated glucose disposal. Results showed that the increment in Rd resulting from the elevation of plasma insulin concentration was relatively minor in NIDDM (38 +/- 6), increasing from a mean (+/- SEM) value of 83 +/- 8 to 121 +/- 12. Similar values in normal subjects were 90 +/- 7 and 274 +/- 26 with an increment of 183 +/- 21. Thus, insulin-stimulated glucose uptake in patients with NIDDM was only one-fifth of that in normals, and accounted for only 31% (38 divided by 121) of total glucose disposal during the clamp study. These data indicate that the majority of previous insulin clamp studies of in vivo insulin action in patients with NIDDM, in which total glucose disposal and insulin-stimulated glucose disposal have been equated, have underestimated the magnitude of insulin resistance present in NIDDM.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Quantitation of insulin-stimulated glucose disposal in patients with non-insulin-dependent diabetes mellitus. 286 88

11 infants with persisting hypoglycemia due to hyperinsulinism (nesidioblastosis of the pancreas) were treated with somatostatin. Somatostatin administration in a relatively high dosage (initially 145 micrograms/m2 body surface as bolus followed by a continuous infusion of the same dose per hour) resulted in a suppression of the circulating insulin concentration leading to a less abrupt fall of the postprandial plasma glucose level. By somatostatin infusion we were able to keep two patients with intractable neonatal hypoglycemia in a normoglycemic state until subtotal pancreatectomy. Infants suffering from nesidioblastosis require 1.0-4.5 micrograms/kg/h somatostatin and a concomitant carbohydrate supply of 0.3-0.48 g/kg/h in order to maintain normoglycemia. An initial somatostatin bolus can be omitted. Somatostatin is very reliable in the treatment of neonatal hypoglycemia due to hyperinsulinism for a limited period of time until subtotal pancreatectomy is performed. In most cases of nesidioblastosis this operative measure seems to be inevitable for the control of hyperinsulinism.
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PMID:[Somatostatin in the emergency treatment of persistent hypoglycemias caused by hyperinsulinism (nesidioblastosis of the pancreas)]. 286 33


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