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)

During mild or moderate nonexhausting exercise, glucose utilization increases sharply but is normally matched by increased glucose production such that hypoglycemia does not occur. To test the hypothesis that redundant glucoregulatory systems including sympathochromaffin activation and changes in pancreatic islet hormone secretion underlie this precise matching, eight young adults exercised at 55-60% of maximal oxygen consumption for 60 min on separate occasions under four conditions: (a) control study (saline infusion); (b) islet clamp study (insulin and glucagon held constant by somatostatin infusion with glucagon and insulin replacement at fixed rates before, during and after exercise with insulin doses determined individually and shown to produce normal and stable plasma glucose concentrations prior to each study); (c) adrenergic blockage study (infusions of the alpha- and beta-adrenergic antagonists phentolamine and propranolol); (d) adrenergic blockade plus islet clamp study. Glucose production matched increased glucose utilization during exercise in the control study and plasma glucose did not fall (92 +/- 1 mg/dl at base line, 90 +/- 2 mg/dl at the end of exercise). Plasma glucose also did not fall during exercise when changes in insulin and glucagon were prevented in the islet clamp study. In the adrenergic blockade study, plasma glucose declined initially during exercise because of a greater initial increase in glucose utilization, then plateaued with an end-exercise value of 74 +/- 3 mg/dl (P less than 0.01 vs. control). In contrast, in the adrenergic blockade plus islet clamp study, exercise was associated with glucose production substantially lower than control and plasma glucose fell progressively to 58 +/- 7 mg/dl (P less than 0.001); end-exercise plasma glucose concentrations ranged from 34 to 72 mg/dl. Thus, we conclude that: (a) redundant glucoregulatory systems are involved in the precise matching of increased glucose utilization and glucose production that normally prevents hypoglycemia during moderate exercise in humans. (b) Sympathochromaffin activation, perhaps sympathetic neural norepinephrine release, plays a primary glucoregulatory role by limiting glucose utilization as well as stimulating glucose production. (c) Changes in pancreatic islet hormone secretion (decrements in insulin, increments in glucagon, or both) are not normally critical but become critical when catecholamine action is deficient. (d) Glucoregulation fails, and hypoglycemia can develop, both when catecholamine action is deficient and when changes in islet hormones do not occur during exercise in humans.
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PMID:Glucoregulation during exercise: hypoglycemia is prevented by redundant glucoregulatory systems, sympathochromaffin activation, and changes in islet hormone secretion. 265 59

We documented stability of plasma glucose concentrations and glucose production and utilization rates, and levels of other metabolic substrates and regulatory factors, during the islet clamp (somatostatin infusion with glucagon and insulin replacement) in the absence of an intervention in five normal humans and further applied this technique to the study of glucoregulation during moderate exercise. Based on previous evidence that sympathochromaffin activation plays a primary role in the prevention of hypoglycemia during exercise, the role of adrenomedullary catecholamines was assessed by exercise (60% of maximum oxygen consumption for 60 min) studies in four bilaterally adrenalectomized, epinephrine-deficient humans under two conditions: control (saline infusion) and islet clamp. Increased glucose utilization and production rates were matched and plasma glucose was unchanged during exercise under both conditions. Thus adrenomedullary catecholamines including epinephrine are not critical to glucoregulation during moderate exercise in humans even when changes in insulin and glucagon are prevented. These findings provide further support for the suggestion that sympathetic neural norepinephrine is the operative catecholamine in the prevention of hypoglycemia during exercise in humans.
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PMID:Epinephrine is not critical to prevention of hypoglycemia during exercise in humans. 265 59

Peripheral plasma concentrations of gastroenteropancreatic peptides were measured during a 3-h period of bicycle exercise at 40% of maximal oxygen uptake in six normal men. Marked increases (P < 0.02) were found in vasoactive intestinal polypeptide (VIP) [1.8 +/- 0.7 (rest) vs. 22.3 +/- 5.4 pmol x l-1 (mean +/- SE) (3 h)], secretin (0.5 +/- 0.5 vs. 11.1 +/- 2.7 pmol x l-1), pancreatic polypeptide (PP) (4.0 +/- 1.5 vs. 46.3 +/- 11.5 pmol x l-1), somatostatin (SRIF) (12.8 +/- 1.2 vs. 17.7 +/- 0.6 pmol x l-1), whereas no changes occurred in gastric inhibitory polypeptide (37.3 +/- 5.9 vs. 39.2 +/- 9.8 pmol x l-1). Immunoreactive insulin and C-peptide decreased from 0.08 +/- 0.004 and 0.39 +/- 0.03 pmol x l-1, respectively, to 0.04 +/- 0.003 (P < 0.005) and 0.13 +/- 0.02 (P < 0.001). The significant decrease in C-peptide and in the C-peptide-to-insulin molar ratio indicate decreased insulin secretion and clearance, respectively, during exercise. Plasma glucose decreased [5.0 +/- 0.1 (rest) vs. 4.2 +/- 0.3 mmol.l-1 (3 h)] (P < 0.01). During 3 h of rest, none of the measured parameters had changed. The marked exercise-induced changes in plasma concentrations of PP, secretin, VIP, and SRIF are provocative. We know in detail neither the stimuli for the release of these peptides nor their physiological role during exercise.
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PMID:Gastroenteropancreatic hormonal changes during exercise. 610 73

We studied the effect of varying oxygen supply on the endocrine and exocrine secretions of the isolated perfused porcine pancreas utilizing completely synthetic perfusion medium with and without the addition of erythrocytes. With synthetic medium oxygenated to a Po2 of 500 mmHg, oxygen consumption was constant for flow rates at or above 0.5 ml x min-1 x g-1 (wet weight). Addition of erythrocytes to the medium did not increase oxygen consumption at flow rates above this level. Furthermore, the secretion of fluid, bicarbonate and protein in response to secretin and acetylcholine was not influenced by addition of erythrocytes. Similarly, the secretion of insulin, glucagon, pancreatic polypeptide, and somatostatin in response to arginine and acetylcholine was unchanged; arginine stimulated the secretion of all four peptides, whereas acetylcholine stimulated the secretion of insulin and pancreatic polypeptide and inhibited glucagon and somatostatin secretion. The results indicate that the porcine pancreas is respiring adequately, when perfused with a completely synthetic perfusion medium at flows above about 0.5 ml x min-1 x g-1 and Po2 about 500 mmHg, and that addition of erythrocytes is not necessary for the study of its secretory functions.
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PMID:Oxygen supply, oxygen consumption, and endocrine and exocrine secretions of the isolated, perfused, porcine pancreas. 610 78

This study compares the gastrointestinal effects of somatostatin (SS) and its putative prohormone, prosomatostatin (Pro-SS), a 28-amino acid peptide isolated from the hypothalamus and the gut, in conscious dogs with chronic gastric and pancreatic fistulae. Pro-Ss suppressed the release of serum gastrin, insulin, and pancreatic polypeptide that occurs in response to feeding a meat meal in a manner similar to that seen with SS. However, in contrast to SS, which strongly reduced intestinal blood flow and oxygen consumption and stimulated intestinal motility, Pro-SS, at the doses tested, had no influence on mesenteric circulation, oxygen uptake, and intestinal motility. We conclude that Pro-SS mimics most of the gastrointestinal secretory actions of SS, but does not exhibit the intestinal circulatory, metabolic, and motor effects of SS.
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PMID:Gastrointestinal secretory, motor, circulatory, and metabolic effects of prosomatostatin. 611 53

Bombesin acts within the anterior hypothalamic preoptic area to interfere with thermoregulation in the rat. The body temperature (Tb) of animals receiving bombesin varies in parallel with ambient temperature (Ta). Bombesin-induced reduction of Tb in animals at low Ta is associated with a marked reduction of oxygen consumption (VO2). Some somatostatin-related peptides, e.g., desAA 1,2,4,5,12,13 [D-Trp8]-somatostatin (ODT8-SS), act within the brain to prevent bombesin-induced reduction of VO2 and Tb. ODT8-SS also produces hyperthermia not associated with an increase in VO2.
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PMID:Bombesin, somatostatin, and related peptides: actions on thermoregulation. 611 85

The effects of somatostatin and vasopressin on blood gases, pulmonary and systemic hemodynamics, and portal pressure assessed by the gradient between occluded and free hepatic vein pressures, were investigated in 18 patients with liver cirrhosis. In the first 10 patients, an iv bolus of 250 microgram somatostatin, followed by an infusion of 125 microgram somatostatin over 30 min, caused a sudden rise in pulmonary and systemic vascular pressures lasting 2 to 5 min and accompanied by bradycardia. There was a slight and transient increase in venous admixture (Qsp/Qt) and alveolar-arterial oxygen tension gradients (P(A-a)O2), and a transient reduction in O2 delivery (O2 del) (-11% of the baseline values) and portal pressures (-14%). In the next 8 patients, vasopressin, 0.4 U/min infused over 30 min, caused a more persistent pulmonary and systemic hypertension and bradycardia, a slight increase in P(A.a)O2 and Qsp/Qt, a reduction in O2 del (-27%) and a decrease in portal pressures (-32%). These effects were marked during the entire vasopressin infusion period. Both somatostatin and vasopressin had vasoconstrictive properties and exerted negative effects on hemodynamics and blood gases. Vasopressin appeared to be a more potent drug than somatostatin.
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PMID:Effect of vasopressin and somatostatin on hemodynamics and blood gases in patients with liver cirrhosis. 612 42

Bombesin and the somatostatin analog, desAA-[D-Trp8]-somatostatin (ODT8-SS), act within the central nervous system to alter animals' oxygen consumption (VO2) in a manner consistent with the observed effects of these peptides on temperature regulation. Bombesin given intracerebroventricularly (i.c.v.) to rats at cold ambient temperatures prevents elevation of VO2 but does not lower VO2 below the values observed at thermoneutrality. ODT8-SS given i.c.v. increases VO2 of animals at an ambient temperature of 20 degrees C and prevents bombesin inhibition of VO2 at low ambient temperatures. Thus, bombesin inhibits VO2 induced by cold and results in hypothermia, ODT8-SS prevents bombesin-induced inhibition of VO2 and bombesin-induced hypothermia and, ODT8-SS increases VO2 and produces hyperthermia in animals at thermoneutral temperatures.
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PMID:Bombesin and somatostatin related peptides: effects on oxygen consumption. 612 48

Cysteamine given subcutaneously to rats decreases brain concentrations of somatostatin-like immunoactivity (SLI) but does not affect vasopressin-like immunoactivity as determined by radioimmunoassay and immunocytochemistry. Since somatostatin-related peptides act within the central nervous system (CNS) to increase body temperature and decrease adrenal epinephrine secretion, changes in these parameters were assessed following cysteamine administration. Cysteamine administration lowers oxygen consumption and body temperature, and elevates plasma concentrations of epinephrine, glucose, insulin and glucagon. The lowering of body temperature and elevation of plasma epinephrine is prevented by CNS administration of the CNS-selective somatostatin analog desAA1,2,4,5,12,13[D-Trp8 ))somatostatin. The CNS actions of somatostatin-related peptides are opposite to the effects of cysteamine. The observations are consistent with the possibility that brain somatostatin-related peptides are involved in regulation of body temperature and adrenal epinephrine secretion.
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PMID:Biological effects of cysteamine: relationship to somatostatin depletion. 613 1

The prevalence of severe dementia in the United States is about 1.3 million cases, of which at least 50 to 60% are of the Alzheimer type. Severe dementia of the Alzheimer type is found rarely in a clearly dominant pattern, although often one or more relatives are affected. Down's syndrome in adults is often associated with Alzheimer changes. The diagnosis is a clinicopathological one; there is a considerable error rate in the clinical diagnosis early in the course of the disease, especially in regard to dementia in depression. The differential diagnosis involves a great many disorders, including multi-infarct dementia, tumors, subdural hematomas, and others. Physiological aspects of Alzheimer's disease include a diffusely slow electroencephalogram, reduced cerebral blood flow, and particular patterns noted on positron emission tomographic scanning. The latter technique has also demonstrated that oxygen extraction is normal in Alzheimer's disease, thus excluding ischemia from possible pathogenetic factors. Morphological changes, that is, the presence of plaques and tangles, are widely distributed in neocortex, paleocortex, and many deep gray areas down through the pontine tegmentum, but largely exclude the basal ganglia, thalamus, and substantia nigra. Numerous plaques without neocortical tangles are found in many demented persons older than 75 years. A severe loss of large neocortical neurons is characteristic of the disease. The chemical nature of the paired helical filaments that make up the neurofibrillary tangle has not yet been ascertained. Neurons are markedly deficient in the basal forebrain nuclei, and this deficiency may account for the severe diminution of choline acetyltransferase and acetylcholine in the neocortex and paleocortex. Muscarinic cholinergic receptors are present in normal amounts. Norepinephrine is reduced in some cases, and somatostatin in most. Substance P is low in severe cases. The etiology of the disorder is unknown and the role of aluminum is disputed. Management of patients with Alzheimer's disease is difficult, and neuroleptics are to be used with great caution because of their side effects. Substrate therapy has not been effective; physostigmine improves memory but is not suitable for general use. Trophic factors, gangliosides, and aluminum chelation are being investigated for use in pharmacological intervention.
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PMID:Senile dementia of the Alzheimer type. 613 75


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