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)

Cigarette smoking is associated with increases in plasma triglycerides and decreases in plasma high density-lipoprotein-cholesterol concentration. These changes not only increase risk of coronary heart disease but also are secondary to resistance to insulin-stimulated glucose uptake or hyperinsulinaemia. To see whether there is a relation between cigarette smoking and insulin-mediated glucose uptake we measured plasma lipid and lipoprotein concentrations, plasma glucose and insulin response to an oral glucose challenge, and insulin-mediated glucose uptake in 40 matched healthy volunteers (20 non-smokers, 20 smokers). Smokers had significantly higher mean (SEM) very-low-density-lipoprotein triglycerides (0.66 [0.10] vs 0.39 [0.03] mmol/l, p less than 0.02) and cholesterol (0.45 [0.06] vs 0.23 [0.04] mmol/l, p less than 0.005) concentrations and lower high-density-lipoprotein cholesterol concentrations (1.16 [0.05] vs 1.51 [0.08] mmol/l, p less than 0.001). Although plasma glucose concentrations in response to the oral glucose load were similar in the two groups, plasma insulin response of the smokers was significantly higher (p less than 0.001). Finally, smokers had higher steady-state plasma glucose concentrations in response to a continuous infusion of glucose, insulin, and somatostatin (8.4 [0.2] vs 5.0 [0.3] mmol/l, p less than 0.001), despite similar steady-state plasma insulin concentrations. The findings show that chronic cigarette smokers are insulin resistant, hyperinsulinaemic, and dyslipidaemic compared with a matched group of non-smokers, and may help to explain why smoking increases risk of coronary heart disease.
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PMID:Insulin resistance and cigarette smoking. 135 97

Patients with hypertension have been shown to be resistant to insulin-stimulated glucose uptake and to be both hyperinsulinemic and hypertriglyceridemic compared with matched normotensive control groups. These abnormalities are present before the institution of antihypertensive therapy and do not necessarily improve when blood pressure is effectively lowered. Insulin resistance, hyperinsulinemia, hypertriglyceridemia, and high blood pressure can be produced in fructose-fed Sprague-Dawley rats, but the development of these changes is inhibited by exercise training or somatostatin infusion. Furthermore, insulin-stimulated glucose uptake is lower in spontaneously hypertensive rats (SHRs) than Wistar-Kyoto rats, and this is associated with higher plasma triglyceride concentrations and blood pressure. In addition, a defect in insulin-stimulated glucose uptake can be shown in adipocytes isolated from SHRs, and the greater the degree of in vitro insulin resistance, the higher the plasma insulin concentration and blood pressure. These data strongly support the view that abnormalities of insulin and lipid metabolism are associated with high blood pressure in both patients and rodent models of experimental hypertension. In the latter context, endogenous hyperinsulinemia and hypertriglyceridemia are risk factors for coronary heart disease. The fact that antihypertensive treatment has not focused on correcting these metabolic abnormalities may explain why it has been difficult to show that lowering blood pressure decreases the risk of coronary heart disease. It can be argued that abnormalities of carbohydrate and lipoprotein metabolism play a role in both the etiology of hypertension and the clinical course of hypertensive patients.
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PMID:Relationship between insulin resistance and hypertension. 174 55

In Taipei, Taiwan, physicians started 13 normally menstruating women on an isocaloric diet (30 kcal/kg; 50% carbohydrate, 30% fat, and 20% protein) and administered a combined triphasic oral contraceptive (OC) to evaluate the effect of the OC on insulin resistance and lipid metabolism including Lp(a) values. (Lp(a) levels may be a risk factor for coronary heart disease.) After three months of taking OCs, the plasma glucose concentration increased significantly (p 0.05). The plasma insulin response to oral glucose was also significantly higher than before OC use (p 0.03). The steady state plasma glucose concentration during constant infusion of glucose, insulin, and somatostatin was much higher three months after OC administration than before OC administration (12.4 vs. 7.5 mmol/l; p 0.001). After three cycles of OC use, the only fasting plasma lipoprotein that increased significantly was triglyceride (0.81 vs. 1.09 mmol/l; p 0.03). The Lp (a) levels stayed essentially the same. OC use decreased significantly the concentration of all serum steroids except DHEAS. These findings indicate that administration of a triphasic low dose OC for three cycles caused glucose intolerance, hyperinsulinemia, and insulin resistance in normal women. It also raised plasma triglyceride concentrations, but did not affect Lp(a) and other lipid values.
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PMID:Prospective evaluation of insulin resistance and lipid metabolism in women receiving oral contraceptives. 813 25

Syncope is defined as a temporary interruption of cerebral perfusion with a sudden and transient loss of consciousness and spontaneous recovery. Approximately one third of the population experiences syncope at least once during a lifetime. Presyncopal signs and symptoms, including weakness, headache, blurred vision, diaphoresis, nausea, and vomiting are sometimes present for seconds or minutes prior to loss of consciousness. After syncope, the patients may present with persisting drowsiness, headache, dizziness, nausea, but not usually confusion. Causes of syncope have been categorized as cardiovascular, non-cardiovascular, and unexplained. Cardiovascular causes can be subdivided into structural heart disease, coronary heart disease, and arrhythmia. Non-cardiovascular causes include neurological, metabolic, psychiatric and other disorders.Orthostatic hypotension - one of the most frequent causes of syncope - has manifold etiologies comprising various neurological and internal diseases. Orthostatic hypotension usually can be attributed to an impairment of peripheral vasoconstriction or to a reduction of the intravascular volume. Signs and symptoms, including the above prodromi are often present just after rising from a supine or sitting position. Frequently, blood pressure decreases significantly without an increase in heart rate. Autonomic cardiovascular modulation is often reduced. Many of the patients with "unexplained" syncope experience neurally mediated (i. e. neurocardiogenic or vasovagal) syncope. In these patients, cardiovascular control may be stable for an extended period of time during orthostatic stress, then there is a sudden decrease in blood pressure and heart rate. Neurocardiogenic or neurally mediated syncope can be associated with painful or emotionally stressful situations such as anxiety or fear, with prolonged standing or specific trigger situations such as micturition, defecation, coughing or sneezing, visceral or carotid sinus stimulation, or with trigeminal or glossopharyngeal neuralgia. So far, the mechanisms of neurocardiogenic syncope are not completely understood. The passive 60 degrees to 70 degrees head-up tilt test is useful for the diagnosis of orthostatic and neurally mediated syncope. The sensitivity of the test can be improved by additional pharmacological provocation, e. g. by isoproterenol, or by increased orthostatic stress using lower body negative pressure stimulation. For the treatment of syncope one should first consider non-pharmacological options. Patients with orthostatic hypotension should avoid rapid changes of the body position from supine to standing, as well as high room temperature or other situations inducing peripheral vasodilatation. An increased intake of sodium and fluids, mild physical exercise or so-called postural counter-maneuvers can improve orthostatic tolerance. Among the drugs recommended for pharmacologic treatment are mineralocorticoids (e. g. fludrocortisone), vasoconstrictor agents (e. g. ephedrine, midodrine), adenosine receptor blockers (theophylline) and beta2-blockers (propanolol), anticholinergic agents, e. g. scopolamine or disopyramide, and negative cardiac inotropes, e. g. beta1-adrenergic blockers or disopyramide. Serotonin reuptake inhibitors (e. g. fluoxetine, sertraline), alpha2-adrenergic agonists (clonidine), central nervous system stimulants such as methylphenidate or phentermine are thought to be beneficial in specific cases. Cardiac pacemakers often seem to be recommended without adequate indication. The antidiuretic, V2-receptor specific, vasopressin analogue desmopressin increases the intravascular volume. Erythropoietin improves anemia and red blood cell decrease and augments blood pressure and cerebral oxygenation. In postprandial hypotension, octreotide, a somatostatin analogue, prostaglandin inhibitors such as indomethacin or ibuprofen, as well as metoclopramide or two cups of coffee per day might be beneficial.
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PMID:[Syncope - a systematic overview of classification, pathogenesis, diagnosis and management]. 1182 26

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

It is well established, that the increased mortality in patients with acromegaly is due to cardiac diseases. Cardiomyopathy is the predominant cardiac alteration in patients with acromegaly. There are less data about coronary heart disease or coronary calcifications. Electron beam computed tomography (EBCT) is the standard imaging modality for identification of coronary artery calcifications (CAC) and can determine the extent and severity of coronary atherosclerosis. Coronary risk was evaluated by the Framingham risk score (FRS). The prospective study included 30 patients with acromegaly (mean age 53+/-14 year; 16 females, 14 males; BMI 28.1+/-3.6 kg/m (2); mean+/-SD), 12 patients had active disease (IGF-1 751+/-338 microg/L; GH 25.6+/-36.4 microg/L), 9 were well-controlled (IGF-1 157+/-58 microg/L; GH 1.8+/-1.1 microg/L) under somatostatin analogue octreotide (n=5), dopamine agonists (n=2), and the GH receptor antagonist pegvisomant (n=2; GH levels were not determined in this subgroup) and 9 were cured IGF-1 (148+/-57 microg/L; GH 0.5+/-0.2 microg/L). Increased left ventricular muscle mass index (LVMI >132 g/m (2)) was focused in 53%, hypercholesterinemia in 63%, hypertension in 43%, diabetes mellitus/impaired glucose tolerance in 27%, and smokers in 53% (pack per year 9+/-15 yr). For quantification of CAC the EBCT was used and the Agatston calcium score was determined. Results were composed to established age and sex adjusted percentile distribution of CAC. CAC was present in 53%, high CAC score (75 (th) percentile) in 37% and were categorized as cardiovascular high risk patients. FRS was related to the CAC score (p=0.008, r (2)=0.22) and the disease duration (p=0.002, r (2)=0.29). The CAC score correlated with LVMI (p=0.02, r (2)=0.17), the disease duration of acromegaly (p=0.004, r (2)=0.36), and the FRS (p=0.008, r (2)=0.22). Patients with a high CAC score had a longer disease duration of 9.6+/-4.7 versus 5.4+/-2.8 years with CAC<75 (th) percentile (p=0.02). In summary, the disease duration and consequently the accompanying metabolic disorders appear to influence the degree of CAC in patients with acromegaly. The observations underline the importance of early and sufficient treatment of acromegaly in high risk patients.
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PMID:Impact of disease duration on coronary calcification in patients with acromegaly. 1937 55