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S Baba

Publications and source records attributed to S Baba.

At least 1,081 records · Page 60Linked to original sources
PubMed1980

Increase of pancreatic somatostatin concentration in early phases of streptozotocin diabetes in rats.

A small yet significant increase of immunoassayable pancreatic somatostatin concentration (0.107 +/- 0.005 vs. 0.156 +/- 0.017 microgram/g at 24 hr, p less than 0.05) was found in rats, 24 hr as well as 7 days after treatment with a diabetogenic dose of streptozotocin (65 mg/kg BW). These animals were characterized by marked decreases of insulin in the pancreas without any significant changes in pancreatic glucagon concentration. These results suggest that an abrupt deprivation of insulin from islets results in an elevation of pancreatic somatostatin concentration, and that glucagon in the pancreas plays a minor role in determining pancreatic somatostatin concentration in rats with insulin-deprived diabetes of short duration.

Animals↗
PubMed1980

Pancreatic islet cell tumors found in rats given alloxan and nicotinamide.

Morphological and biochemical studies were performed in pancreatic islet cell tumors found in rats given alloxan (40 mg/kg) and nicotinamide (305 mg/kg). Complete serial sections of the whole pancreas, combined with planimetric analysis, uncovered islet cell tumors in 5 of 7 rats which were killed 10 to 14 months after treatment. Hypoglycemia associated with hyperinsulinemia was found in a rat which developed a tumor which consisted of cells which reacted lightly with aldehyde fuchsin. Another rat developed a gross tumor which was composed of cells stained deeply with aldehyde fuchsin. However, flat insulin response to glucose associated with glucose intolerance was found in this rat. In addition to B cells, a few A and D cells were found within the two tumors. The present study suggests that pancreatic islet cell tumors found in rats given alloxan and nicotinamide are composed of at least three endocrine cell populations, although the majority of tumor cells are insulin-producing B cells.

Adenoma, Islet Cell↗
PubMed1980

Pancreatic insulin, glucagon and somatostatin concentrations in rats with islet cell tumors induced by streptozotocin.

Hyperinsulinemic and hypoglycemic rats with islet tumors induced by streptozotocin were shown to have significantly decreased immunoreactive insulin and somatostatin concentration (expressed as per g wet weight (w. wt) and content (expressed as per whole pancreas) in the pancreas surrounding the tumor as compared to those of age and weight adjusted controls. The pancreatic glucagon concentration of the former was significantly lower than that of the latter but no significant difference between glucagon content in the two groups was observed. Thus, inverse relationships were demonstrated between circulating insulin and somatostatin as well as insulin in the pancreas. It is suggested that a large amount of insulin in plasma results in a decrease in pancreatic insulin and somatostatin.

Adenoma, Islet Cell↗
PubMed1980

Portal somatostatin responds to intragastric glucose: effects of streptozotocin diabetes.

Changes in somatostatin levels in portal response to intragastric glucose loading were examined in normal controls and streptozotocin diabetic rats for one week duration. The mean (+/- SEM) basal level of somatostatin was more significantly elevated in diabetic rats (401 +/- 62 pg/ml) than in controls (171 +/- 13 pg/ml). However, no significant difference in somatostatin concentrations 30 min after glucose loading was found between diabetic and control animals (587 +/- 113 vs. 443 +/- 47 pg/ml). Glucose loading caused a significant elevation of somatostatin in controls, but not in diabetic rats. These results suggest a physiologic role of somatostatin in nutrient homeostasis, and that abnormalities in D cell function are present in streptozotocin diabetes of short duration.

Animals↗
PubMed1980

Effect of propranolol on glucose-induced insulin response in rats with insulinomas.

This paper describes an inhibitory effect of propranolol on insulin secretion in rats with pancreatic islet cell tumors which have been induced by streptozotocin (65 mg/kg body weight) and nicotinamide (500 mg/kg). Following glucose ingestion (3 g/kg), propranolol (4 mg/kg) was injected into the tumor-bearing rats. Plasma insulin decreased paradoxically despite an increase in blood glucoses. In contrast, propranolol did not suppress insulin secretion in normal rats. The drug was found to have no effect on glucagon secretion in either experimental or control animals during glucose load. This may suggest that the experimentally induced insulinoma in hypersensitive to propranolol for inhibiting insulin secretion.

Adenoma, Islet Cell↗
PubMed1980

Role of glucagon and somatostatin in insulin release.

The role of endogenous glucagon and somatostatin in insulin release was studied. Islets isolated from adult rats were incubated for 60 min in 3.3, 8,3 and 16.7 mM glucose with anti-glucagon antiserum (AGA) or anti-somatostatin antiserum (ASA) which was produced in rabbits. For the control experiments the antiserum was replaced by normal rabbit serum (NRS). Insulin release from islets treated with AGA was suppressed in 3.3 and 8.3 mM glucose as compared to islets treated with NRS, while insulin release was not affected in 16.7 mM glucose. On the other hand, insulin release from islets treated with ASA was enhanced in 3.3 and 8.3 mM glucose as compared to that from islets treated with NRS, whereas in 16.7 mM glucose it was not different from the control. These observations indicate that endogenous glucagon and somatostatin play a physiological role in the regulation of insulin release, but their regulation of insulin release is deranged at non-physiologically high glucose concentrations.

Animals↗
PubMed1980

Effect of somatostatin and calcium deprivation on cholecystokinin or caerulein-induced insulin and glucagon release from the isolated perfused rat pancreas.

The present experiments were undertaken to investigate the effect of alteration in on extracellular calcium concentration and of somatostatin on cholecystokinin-(CCK)- and caerulein-induced insulin and glucagon release from the isolated perfused rat pancreas. In control studies using perfusate containing 2.5 mM CaCl2 and 50 mg/dl glucose, CCK and caerulein caused insulin and glucagon release in a dose-related fashion. During perfusion with calcium free medium, insulin release was markedly inhibited. Subsequent introduction of 2.5 mM CaCl2 to the medium restored insulin response toward control levels. Extracellular calcium depletion, however, had no effect on CCK- or caerulein-induced glucagon release. The output of glucagon in the absence of calcium was comparable to that seen in the control experiments. On the other hand, somatostatin abolished the increase in glucagon secretion, but not the increase in insulin secretion, when perfused simultaneously with CCK or caerulein. However, pretreatment for 10 min with somatostatin blocked even insulin secretion. However, pretreatment for 10 min with somatostatin blocked even insulin secretion. The effects of somatostatin on hormonal discharge are suggested to be related to an alteration in the handling of or response to calcium. Recently, somatostatin has also been shown to inhibit calcium uptake by islets. Thus, the present results indicate a differential sensitivity of CCK- and caerulein-stimulated alpha and beta cell to extracellular calcium depletion and to the effect of somatostatin.

Animals↗
PubMed1980

Somatostatin concentration responds to arginine in portal plasma: effects of fasting, streptozotocin diabetes, and insulin administration in diabetic rats.

Changes of somatostatin concentration in response to a single i.v. injection of arginine (400 mg/kg body weight) were examined in extracted portal plasma of normal and diabetic rats in the fully fed state and after 24 h or fasting, as well as in diabetic rats treated with insulin for one week. In both normal and diabetic animals fasted for 24 h, the basal level of somatostatin declined but the magnitude of the arginine-induced elevation of somatostatin was not affected, suggesting a physiologic role of the tetradecapeptide in nutrient homeostasis. When compared with intact rats, diabetic animals were shown to have increased levels of somatostatin before and after arginine administration, both of which were attenuated by insulin replacement therapy. These findings suggest that alterations of D cell function in streptozotocin diabetes may be related to either insulin deficiency or its metabolic consequences.

Animals↗
PubMed1980

Immunochemical studies on the insulin-degrading enzyme from pig and rat skeletal muscle.

Insulin-degrading enzyme (IDE), which proteolytically degraded insulin with a high degree of specificity, was purified from pig skeletal muscle by ammonium sulfate precipitation, chromatography on Bio-Gel P-200 and DEAE-cellulose, and finally rechromatography on Sephadex G-200 (rechromatography fraction). The enzyme was also purified by affinity chromatography (affinity fraction). Both fractions migrated as a single component at the same position on polyacrylamidegel disc electrophoresis. Antiserum against pig muscle IDE was obtained by immunization of rabbits using the rechromatography fraction. By means of antiserum, it was shown that pig muscle IDE (affinity fraction), rat muscle cytosol-, and membrane-IDE gave a precipitin band of identity in Ouchterlony double-immunodiffusion systems. Quantitative immunoprecipitin data demonstrated that the antiserum inhibited the activities of the above three IDEs compared with normal rabbit serum. These data suggest that the insulin-degrading enzyme from porcine muscle and that from rat muscle have similar immunologic properties. The antiserum described here should be a useful tool for the examination of subcellular distribution and the quantitative analysis of insulin-degrading enzyme. It may also be helpful in determining the physiologic significance of IDE.

Animals↗
PubMed1980

Site-specific deuteration of tyrosine and their assay by selective ion monitoring method.

L-[2',3',5',6'-d]Tyrosine (Tyr-d4) and L-[2',6'-d[Tyr (Tyr-d2) were prepared. Tyr was heated in conc. DCl at 180 degrees C for 4 hr to obtain DL-[2,2',3',5',6'-d]Tyr (Tyr-d5), then the deuterium on the 2-position of the compound was successfully replaced with proton by refluxing with an acetic acid-acetic anhydride mixture. The isotopic purity of DL-Tyr-d4 was aobut 60%. The racemic mixture was resolved enzymatically. L-Tyr-d2 was prepared by refluxing the resultant Tyr-d4 with 5.5N HCl. The deuterated amino acids were analyzed as the N,)-bis (trifluoroacetyl) methyl ester of N,O-bis(heptafluorobutyryl) methyl ester derivatives by the gas chromatography-selective ion monitoring method (SIM). The calibration curves showed good linearity in the range where the molar ratios of Tyr-d4/Ttr-d0 and Tyr-d2/Tyr-d0 were above 5/1,000. The results indicate that the protein-bound Tyr-d4 may possibly be determined as Tyr-d2 after hydrolysis of protein.

Chromatography, Gas↗
PubMed1980

Wegener's granulomatosis with intracerebral granuloma and mammary manifestation. Report of a case.

A 48-year-old woman was examined who had a limited form of Wegener's granulomatosis with neurologic manifestations. Despite the relative frequency of neurologic manifestations, we found only two other cases in the literature in which intracerebral granulomas were involved. Moreover, mammary manifestations with necrotizing granulomas developed in this case. Glucocorticoid treatment was effective because the case showed both brain and mammary involvement. This case was uncommon in that the intracerebral and mammary granulomas developed in an area remote from that usually affected by Wegener's granulomatosis.

Brain Diseases↗