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Arsélio P. Carvaho - One of the best experts on this subject based on the ideXlab platform.
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Stimulation of Immunoreactive Insulin release by glucose in rat brain synaptosomes.
Neurochemical research, 1999Co-Authors: Maria S. Santos, Emilia M. Pereira, Arsélio P. CarvahoAbstract:The effect of glucose on the release of Immunoreactive Insulin (IRI) in synaptosomes isolated from rat brain was studied. In the absence of glucose synaptosomes release about 4% (0.77 μIU/mg protein) of total content. Glucose increases significantly the IRI released by synaptosomes. Addition of the glycolytic inhibitor iodoacetic acid (IAA), decreased the glucose-induced release of IRI by about 50%, suggesting that glucose metabolism is involved. The observation that glucose provides a concentration related signal for IRI release indicates that this synaptosomal preparation may be useful as a model for research on the mechanism of Insulin release in brain.
G E Bauer - One of the best experts on this subject based on the ideXlab platform.
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Immunoreactive Insulin in rat salivary glands and its dependence on age and serum Insulin levels
Experimental Biology and Medicine, 1995Co-Authors: D A Carter, J D Wobken, Padmakar K Dixit, G E BauerAbstract:The major salivary glands of adult rodents contain Immunoreactive Insulin (IRI). To determine if the concentration of IRI in salivary glands is modulated by the level of serum Insulin, Insulin immunoreactivity in the parotid and submandibular glands of male rats at different ages (sucklings, pubescent, mature, and elderly) was assayed and compared with corresponding serum Insulin concentrations. Salivary glands from suckling rats contained 94 ng/g (wet weight) Insulin, which is 1.6 times higher than the level in pubescent rats, and about 10 times higher than levels in mature and elderly rats. No direct relationship between salivary gland content and serum IRI levels was indicated by the data. In an attempt to increase Insulin levels in serum, Insulin-secreting pancreatic islet adenomas were induced in young male rats by injecting streptozotocin (an islet tumor-inducing drug) with nicotinamide (which reduces the drug's beta-cell cytotoxicity). The mean Insulin content of salivary glands from drug-treated rats that had not yet expressed tumors was no higher than controls. After the development of visible tumors of pancreatic islet tissue, however, salivary gland IRI was markedly elevated, reaching 40 times control levels, whereas serum Insulin, and the Immunoreactive Insulin content of two Insulin-sensitive tissues (vis. hepatic, adipose), were elevated only 2-fold. Examination of histologic sections of the parotid and submandibular glands from drug-treated animals revealed no evidence for the formation of salivary tumors. The data indicate that salivary gland Insulin content (i) is age-related, being highest in neonates and declining thereafter, (ii) is generally identical in parotid and submandibular glands at a given age, and (iii) is not modulated solely by the animal's serum Insulin concentration. These results are discussed in regard to the possible sources of Insulin detected in the major salivary glands.
Maria S. Santos - One of the best experts on this subject based on the ideXlab platform.
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Stimulation of Immunoreactive Insulin release by glucose in rat brain synaptosomes.
Neurochemical research, 1999Co-Authors: Maria S. Santos, Emilia M. Pereira, Arsélio P. CarvahoAbstract:The effect of glucose on the release of Immunoreactive Insulin (IRI) in synaptosomes isolated from rat brain was studied. In the absence of glucose synaptosomes release about 4% (0.77 μIU/mg protein) of total content. Glucose increases significantly the IRI released by synaptosomes. Addition of the glycolytic inhibitor iodoacetic acid (IAA), decreased the glucose-induced release of IRI by about 50%, suggesting that glucose metabolism is involved. The observation that glucose provides a concentration related signal for IRI release indicates that this synaptosomal preparation may be useful as a model for research on the mechanism of Insulin release in brain.
T D R Hockaday - One of the best experts on this subject based on the ideXlab platform.
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the relationship between obesity plasma Immunoreactive Insulin concentration and blood pressure in newly diagnosed indian type 2 diabetic patients
Diabetic Medicine, 1993Co-Authors: C S Yajnik, S S Naik, Dattatray S Bhat, V M Joshi, K M Shelgikar, K G M M Alberti, T D R HockadayAbstract:The association of blood pressure with clinical and biochemical measures was studied in 185 newly diagnosed Type 2 diabetic patients, 74 impaired-glucose-tolerant (IGT) and 128 non-diabetic control subjects. Hyperglycaemic subjects were older than control subjects (controls 40 (24–59) years, IGT 48 (29–64) years, diabetic 43 (29–60) years, median (5th-95th centile) both p < 0.05). They were also more obese (body mass index (BMI) controls 23.5 kg m−2 (17.2–29.9), IGT 26.0 kg m−2 (19.8–33.9), diabetic 24.2 kg m−2 (19.3–32.2)) and with a greater waist-hip ratio (controls 0.83 (0.70–0.98), IGT 0.88 (0.75–0.98), diabetic 0.89 (0.75–1.00)). Blood pressure was significantly higher in both IGT (systolic 127mmHg (108–162), diastolic 80 mmHg (66–99)) and diabetic patients (systolic 130 mmHg (104–160), diastolic 84 mmHg (66–102)) compared to non-diabetic controls (systolic 120 mmHg (100–151), diastolic 80 mmHg (60–94)). Univariate analysis showed that in diabetic patients systolic blood pressure was related to age (r = 0.17, p < 0.05), BMI (r= 0.23, p < 0.01) and plasma Immunoreactive Insulin (fasting and post glucose, r= ˜ 0.25, p<0.01) but not to C-peptide concentrations; diastolic blood pressure to BMI (r= 0.35, p < 0.001), waist-hip ratio (r = 0.23, p < 0.01) and plasma Immunoreactive Insulin (fasting r= 0.30, p < 0.001, post glucose r = ˜ 0.20, p < 0.05) but not to C-peptide concentrations. Multivariate analysis revealed that systolic blood pressure in diabetic patients was related to BMI (p < 0.01) and fasting Immunoreactive Insulin (p < 0.05) while diastolic blood pressure was related to BMI (p < 0.001) and waist-hip ratio (p < 0.01). Thus, blood pressure is associated with obesity even in our relatively non-obese population and it is also associated with plasma Immunoreactive Insulin concentrations. The mechanism of these associations remains to be established.
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The relationship between obesity, plasma Immunoreactive Insulin concentration and blood pressure in newly diagnosed Indian type 2 diabetic patients
Diabetic medicine : a journal of the British Diabetic Association, 1993Co-Authors: C S Yajnik, S S Naik, Dattatray S Bhat, V M Joshi, K M Shelgikar, K G M M Alberti, T D R HockadayAbstract:The association of blood pressure with clinical and biochemical measures was studied in 185 newly diagnosed Type 2 diabetic patients, 74 impaired-glucose-tolerant (IGT) and 128 non-diabetic control subjects. Hyperglycaemic subjects were older than control subjects (controls 40 (24–59) years, IGT 48 (29–64) years, diabetic 43 (29–60) years, median (5th-95th centile) both p < 0.05). They were also more obese (body mass index (BMI) controls 23.5 kg m−2 (17.2–29.9), IGT 26.0 kg m−2 (19.8–33.9), diabetic 24.2 kg m−2 (19.3–32.2)) and with a greater waist-hip ratio (controls 0.83 (0.70–0.98), IGT 0.88 (0.75–0.98), diabetic 0.89 (0.75–1.00)). Blood pressure was significantly higher in both IGT (systolic 127mmHg (108–162), diastolic 80 mmHg (66–99)) and diabetic patients (systolic 130 mmHg (104–160), diastolic 84 mmHg (66–102)) compared to non-diabetic controls (systolic 120 mmHg (100–151), diastolic 80 mmHg (60–94)). Univariate analysis showed that in diabetic patients systolic blood pressure was related to age (r = 0.17, p < 0.05), BMI (r= 0.23, p < 0.01) and plasma Immunoreactive Insulin (fasting and post glucose, r= ˜ 0.25, p
Erkka Syvälahti - One of the best experts on this subject based on the ideXlab platform.
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The levels of serum growth hormone and Immunoreactive Insulin after administration of antipyretic analgetics.
Acta pharmacologica et toxicologica, 2009Co-Authors: Erkka SyvälahtiAbstract:: The effects of indomethacin (100 mg) and phenylbutazone (250 mg) suppositories and acetylsalicylic acid (1000 mg) as well as placebo tablets on serum growth hormone, serum Immunoreactive Insulin and blood glucose concentrations were studied in young male volunteers after an overnight fast. Peak drug concentration in serum was reached 60, 120, and 180 minutes after indomethacin (2.1 ± 0.3 μg/ml), acetylsalicylic acid (88.0 ± 13.4 μg/ml) and phenylbutazone (30.8 ± 2.2 μg/ml), respectively. Blood glucose rose from 4.2 ± 0.1 mmol/l to 5.0 ± 0.1 mmol/l (P < 0.001) (n = 21) at 120 minutes after indomethacin and the rise was significant throughout the study. No significant changes in blood glucose were seen after the administration of the other drugs. The levels of serum growth hormone were also significantly increased after indomethacin throughout the study, but not after the other drugs. The mean of the peak serum growth hormone concentration of the subjects (11.7 ± 1.2 ng/ml) (n = 19) was significantly higher after indomethacin than after the other drugs, which did not not differ from each other significantly. There were no significant changes in serum Immunoreactive Insulin levels after the drugs. However, after acetylsalicylic acid the levels tended to increase and the serum Immunoreactive Insulin remained significantly higher at 30, 60, and 120 minutes after acetylsalicylic acid (18.5 ± 1.6, 19.1 ± 3.4, and 20.2 ± 3.2 μU/ml) (n = 13) than after placebo (11.2 ± 2.2, 10.1 ± 2.0, and 10.6 ± 1.5 μU/ml) (n = 13) (P < 0.05).
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Serum Growth Hormone, Serum Immunoreactive Insulin and Blood Glucose Response to Intravenous Tolbutamide in Postmenopausal Women with and without Natural Oestrogen Therapy
Acta pharmacologica et toxicologica, 2009Co-Authors: Erkka Syvälahti, Risto Erkkola, Reijo Punnonen, L. RauramoAbstract:The response of serum growth hormone, serum Immunoreactive Insulin and blood glucose to intravenously administered tolbutamide was studied in twenty non-obese and four obese healthy volunteer postmenopausal women with or without oestrogen therapy. Fasting blood glucose and the maximal fall in blood glucose during the test (44 % and 45 %) was normal in the non-obese control and oestrogen groups, and the two groups did not differ significantly from each other. Even the four obese women, two on oestrogen therapy and two without, showed a normal blood glucose response to tolbutamide. Moreover the response of serum Immunoreactive Insulin to tolbutamide was normal in subjects both with and without oestrogen therapy and there were no significant differences between the two groups. The response of serum growth hormone to tolbutamide was small in both groups, but slightly more pronounced in the non-obese women undergoing oestrogen therapy than in the controls. It is concluded that a postmenopausal period of five years leads to no impairment in carbohydrate metabolism in healthy women, and an oestrogen therapy for 3–7 years has no effects on glucose tolerance in healthy postmenopausal subjects.
