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T Taminato

Publications and source records attributed to T Taminato.

At least 19 recordsLinked to original sources
PubMed1992

Lactate dehydrogenase (LDH)-linked immunoglobulin in a patient with Graves' disease treated with methimazole.

A 26-year-old woman who received methimazole treatment for Graves' disease is discussed. Two months following treatment, her serum GOT level rose to 45 K.U, her GPT to 60 K.U, and her lactate dehydrogenase (LDH) to 645 W.U; a hepatic disorder was then suspected. Later, the serum GOT and GPT concentrations decreased to a normal range, but her serum LDH continued to maintain a high level. An LDH isoenzyme analysis showed an abnormally broad LDH. The IgG that was linked to the LDH is suspected to have been the result of her underlying autoimmunity, the methimazole treatment, and the development of her hepatic disorder. Thus, this IgG was thought to be the autoantibody to LDH.

Adult↗
PubMed1992

Role of cytosolic Ca2+ in impaired sensitivity to glucose of rat pancreatic islets exposed to high glucose in vitro.

Sustained exposure to high concentrations of glucose selectively impairs the ability of pancreatic islets to secrete insulin in acute glucose stimulation. In order to evaluate the interrelationship between impaired insulin secretion and the dynamics of the cytosolic free Ca2+ level ([Ca2+]i), we have investigated the effect of high glucose exposure on both [Ca2+]i dynamics in single rat beta-cells and insulin release from rat pancreatic islets. Islets cultured at a high glucose concentration (16.7 mM) for 24 h showed significant reductions of the 16.7 mM GSIR compared with islets cultured at a normal glucose concentration (5.5 mM) (3.38 +/- 0.24 vs. 4.26 +/- 0.34%, respectively, P < 0.05). The capacity of glucose to raise the [Ca2+]i level also was significantly reduced in the beta-cells maintained for 24 h at 16.7 mM glucose (P < 0.001). An additional culture in the medium with 5.5 mM glucose for 16 h restored both the GSIR and the [Ca2+]i response of islets cultured at high glucose. On the other hand, insulin release and [Ca2+]i rise in response to 20 mM L-Arg were well preserved. These observations confirm that exposure of pancreatic beta-cells to high glucose concentrations induces a selective reduction of the GSIR and, further, shows that this impaired response is reversibly restored by an additional culture with normal glucose. We also suggest that the inability of glucose to provoke a [Ca2+]i rise, which is observed in the beta-cells exposed to high glucose, may be responsible for the selective impairment of the GSIR.

Animals↗
PubMed1990

Mechanism of sympathetic neural regulation of insulin, somatostatin, and glucagon secretion.

The effects of electrical stimulation of the left splanchnic nerve on insulin, somatostatin, and glucagon secretion from the isolated perfused rat pancreas were investigated. Electrical splanchnic nerve stimulation (SNS), performed by square-wave impulses, produced a 25% decrease in effluent flow and a 10-fold increase in perfusate norepinephrine. Both insulin and somatostatin output in the presence of 16.7 mM glucose were inhibited during SNS by 85 and 56% of the basal value, respectively. Glucagon output in the presence of 5.5 mM glucose was stimulated 20-fold by SNS. Perfusion with 10(-6) M propranolol further decreased insulin and somatostatin output during SNS, when expressed as the total decrement beneath basal during stimulation. The glucagon response to SNS tended to be enhanced, although not significantly, by simultaneous infusion of 10(-6) M propranolol. However, 10(-6) M phentolamine (Phe) attenuated the SNS-induced inhibition of insulin and somatostatin output by 50 and 40%, respectively. However, insulin output remained decreased after SNS with Phe. The SNS-induced glucagon response was completely abolished by 10(-6) M Phe alone or by 10(-6) M Phe plus 10(-6) M propranolol. With 10(-6) M Phe plus 10(-6) M propranolol, insulin and somatostatin output remained decreased after SNS. These results suggest that insulin and somatostatin secretions induced by glucose are inhibited during SNS through the alpha-adrenergic mechanism and also that the beta-adrenergic mechanism exerts a stimulatory action. SNS-induced glucagon secretion occurs mainly through alpha-adrenergic activation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Importance of imparied insulin-gene expression in occurrence of diabetes in obese rats.

To investigate the role of the beta-cell in the occurrence of diabetes in obesity, longitudinal changes of insulin-gene expression and pancreatic insulin content were compared among genetically obese diabetic (Wistar fatty) rats, genetically obese nondiabetic (Zucker fatty) rats, and ventromedial hypothalamus (VMH)-lesioned obese rats. Plasma glucose levels were significantly elevated with age in Wistar fatty rats, whereas they were virtually unchanged in VMH-lesioned and Zucker fatty rats. Obesity and hyperinsulinemia were evident in VMH-lesioned rats 1 wk after the operation and in Zucker and Wistar fatty rats at 5 wk of age. In VMH-lesioned rats, the pancreatic preproinsulin I mRNA (pplmRNA) level and pancreatic insulin content markedly increased approximately two- to threefold (P less than 0.001) with the development of hyperinsulinemia, whereas sham-operated rats showed no significant change. In Zucker and Wistar lean rats, the pplmRNA level and pancreatic insulin content increased with age, corresponding to increases in body weight. In Zucker fatty rats, the pplmRNA level and pancreatic insulin content at 5 and 14 wk of age were significantly higher than those of lean littermates. The pplmRNA level in Zucker fatty rats at 14 wk of age reached 290% of that of their lean littermates (P less than 0.001). On the other hand, the pplmRNA level and pancreatic insulin content in Wistar fatty rats at 5 and 14 wk of age did not increase more than those of their lean littermates at the corresponding ages and were therefore significantly lower than in Zucker fatty rats, which had a higher grade of hyperinsulinemia at 14 wk of age.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Short term effects of glucose and arginine on the preproinsulin messenger ribonucleic acid level in the perfused rat pancreas: comparison with insulin secretion.

To investigate the role of glucose and arginine in short term regulation of preproinsulin mRNA (ppImRNA) levels, the rat pancreas was perfused in the presence of glucose and/or arginine, and changes in ppImRNA levels in the pancreas were compared with the amount of insulin released during the perfusion. Perfusion of the pancreas with high glucose and arginine induced a significant increase in ppImRNA levels within 2 h, whereas perfusion with low glucose and arginine or high glucose alone had no significant effect during this period. The insulin release induced by perfusion of high glucose combined with arginine was 2 times greater than that induced by high glucose alone or low glucose with arginine. In conclusion, insulin gene transcription can be evoked during a short period in response to an extremely large secretory demand for insulin.

Animals↗
PubMed1988

Characteristic features of insulin secretion in the streptozotocin-induced NIDDM rat model.

Male Wistar neonatal rats at age 1.5 days (Streptozotocin [STZ] group 1) and 5 days (STZ group 2) received a subcutaneous injection of 90 mg/kg STZ. After 10 weeks, the rats were subjected to an oral glucose tolerance test (OGTT) (2 g/kg) in a conscious state. The pancreas perfusion experiments were conducted 2 weeks after the OGTT. There was no statistical difference in insulin response between the STZ group 1 and the control group. On the contrary, in the STZ group 2, the plasma glucose response to OGTT showed a typical diabetic pattern, and the plasma insulin response was markedly blunted. In the isolated perfused rat pancreas, the infusion of glucose evoked a biphasic insulin secretion, but the peak insulin levels induced by 16.7 mmol/L glucose in the STZ group 1 were significantly lower than in the controls. We further investigated characteristics of insulin secretion in response to different secretagogues in these animal models using isolated islets. The insulin content of the islets of the STZ group 1 were about one half that of the control group. Insulin secretion in the STZ group 1 was impaired in response to glucose stimulation, but remained normal in response to arginine and forskolin. These results suggest that insulin secretion of non-insulin-dependent diabetes mellitus (NIDDM) rat model is selectively impaired in response to glucose stimulation, possibly due to a disorder of signaling mechanism other than adenylate cyclase.

Animals↗
PubMed1988

Comparative effect of somatostatin-14 and somatostatin-28 on glucagon-induced glycogenolysis from the perfused rat liver.

The effect of somatostatin (SS)-14 and SS-28 on glycogenolysis was studied, using a rat liver perfusion technique. Livers from nonfasted rats were perfused with 5.5 mmol/L glucose or perfusate without the glucose addition. Glucagon-induced glucose output was lower in the presence of 5.5 mmol/L glucose than in glucose free perfusate at every concentration of glucagon. Under glucose free conditions, SS-14 given at five minutes prior to the glucagon addition reduced the glucagon-induced glucose output dose-dependently. SS-14 given 15 minutes after glucagon addition also inhibited glucagon-induced glucose output significantly. However, various concentrations of SS-28 failed to affect glucose output. On the other hand, in the presence of 5.5 mmol/L glucose, neither SS-14 nor SS-28 affected glucagon-induced glucose output. It is suggested, therefore, that glycogenolysis induced by glucagon from the liver is reduced by SS-14, but not by SS-28, only under glucose free conditions.

Animals↗
PubMed1988

Detection of antibodies against wheat germ agglutinin bound glycoproteins on the islet-cell membrane.

An attempt was made to detect islet cell surface antibodies (ICSAb) using solubilized islet-cell glycoproteins as antigens. Isolated rat islets were labelled with 125I-wheat germ agglutinin (WGA) and solubilized by Nonidet P-40 with sonication. 125I-WGA-bound islet-cell proteins were incubated with test sera, and bound antibodies were precipitated with anti-human IgG or IgM immunobeads. Serum which had a bound percent beyond the mean plus 2SD of control sera was defined as antibody-positive. Results obtained by this method correlated well with those by the immunofluorescence method of detecting ICSAb. Prevalences of antibodies were 21/114 (18%) for IgG antibodies and 9/114 (8%) for IgM antibodies in patients with insulin-dependent diabetes mellitus (IDDM). The prevalence was highest for both IgG and IgM antibodies in patients within a year of the onset of disease (38 and 25%, respectively), and decreased thereafter. The prevalence of IgM antibodies was lower than that of IgG antibodies at all stages. In NIDDM patients, the prevalence of antibodies was 5/72 (7%) for both IgG and IgM antibodies. If these preliminary results are confirmed, this radioassay may be developed to detect antibodies against islet cell membrane proteins on a large scale.

Animals↗
PubMed1988

Degradation and conversion of somatostatin in normal and diabetic rats in vivo and in vitro.

Plasma somatostatin-like immunoreactivity in the portal and jugular veins of streptozotocin diabetic rats was compared with that in normal control rats. In the diabetic group, somatostatin levels in the portal (p less than 0.05) and jugular (p less than 0.01) veins were both elevated compared with those in the control group. Moreover, the degree of elevation was greater in the jugular vein than in the portal vein. To further investigate the role of the liver in the clearance of somatostatin-28 in vivo, 2 micrograms of somatostatin-28 was administered as a bolus into the external jugular vein of intact and functionally hepatectomized rats. The mean half-time of somatostatin-28 was significantly longer in intact diabetic rats than in controls (p less than 0.05). The functional hepatectomy did not cause a significant difference in the half-time in diabetic rats but made it longer in control rats. These results suggest that the longer half-time of somatostatin-28 in diabetic rats in vivo is due to its slower hepatic clearance. The hepatic clearance of somatostatin-28 and somatostatin-14 was further studied in vitro using a recirculating liver perfusion method. The hepatic clearance of 1.2 nM of either somatostatin-28 or somatostatin-14 was significantly lower in diabetic rats than in controls (p less than 0.01). This indicates that elevated plasma somatostatin levels in diabetic rats are caused at least in part by decreased hepatic clearance of somatostatin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Effects of naloxone on basal and vagus nerve-induced secretions of GRP, gastrin, and somatostatin from the isolated perfused rat stomach.

The effects of naloxone, an opiate antagonist, on basal and vagus nerve-induced secretions of GRP, gastrin, and somatostatin were examined using the isolated perfused rat stomach prepared with vagal innervation. Naloxone (10(-6) M) significantly inhibited basal somatostatin secretion in the presence and absence of atropine and of hexamethonium, whereas basal GRP and gastrin secretion was not affected by naloxone. Electrical stimulation (10 Hz, lms duration, 10V) of the distal end of the subdiaphragmatic vagal trunks elicited a significant increase in both GRP and gastrin but a decrease in somatostatin. Naloxone (10(-6) M) failed to affect these responses in the presence or absence of atropine. On the other hand, when hexamethonium was infused, naloxone significantly inhibited both the GRP and gastrin responses to electrical vagal stimulation. Somatostatin secretion was unchanged by vagal stimulation during the infusion of hexamethonium with or without naloxone. These findings suggest that basal somatostatin secretion is under the control of an opiate neuron and that opioid peptides might be involved in vagal regulation of GRP and gastrin secretion.

Animals↗
PubMed1987

Effect of the alpha 2-blocker DG-5128 on insulin and somatostatin release from the isolated perfused rat pancreas.

2[2-(4.5-Dihydro-1H-imidazol-2-yl)-1-phenylethyl] pyridine dihydrochloride sesquihydrate (DG-5128) is an alpha 2-specific-adrenergic antagonist. We have studied the effect of DG-5128 on insulin and somatostatin release from the isolated perfused rat pancrease. DG-5128 stimulated somatostatin and insulin release not only at a low glucose concentration but also at a high glucose concentration. These findings suggest that an alpha 2-adrenergic receptor plays an important role in the regulation of insulin and somatostatin secretion.

Animals↗
PubMed1987

Vagal regulation of insulin, glucagon, and somatostatin secretion in vitro in the rat.

Using a new in vitro procedure of the isolated perfused rat pancreas with vagal innervation, electrical vagal stimulation produced an increase in both insulin and glucagon secretion in proportion to the pulse frequency, but an inhibition in somatostatin release. When atropine was infused, both insulin and glucagon responses to vagal stimulation were partially suppressed, whereas somatostatin release was enhanced. In the presence of hexamethonium, vagal stimulation failed to affect insulin, glucagon, or somatostatin secretion. Propranolol partially blocked both insulin and glucagon responses but did not influence somatostatin response. Phentolamine had no significant effect on release of hormones. Simultaneous administration of propranolol and phentolamine tended to inhibit both insulin and glucagon responses to vagal stimulation. These findings suggest that not only a cholinergic but also a noncholinergic neuron may be involved in vagal regulation of pancreatic hormone secretion and that these neurons may be under the control of preganglionic vagal fibers via nicotinic receptors.

Animals↗
PubMed1986

A functional study of a case of glucagonoma exhibiting typical glucagonoma syndrome.

A 46-year-old man had a 7-year history of severe rash, which was then diagnosed as necrolytic migratory erythema. He had a weight loss of 6 kg, abnormal glucose tolerance test findings, anemia, glossitis, hair loss, and hypoproteinemia. Plasma amino acids levels were significantly decreased, and the fasting plasma glucagon (IRG) level was high at 5000 to 8000 pg/ml. Circulating IRG significantly increased after oral glucose loading, meal ingestion, and arginine infusion, and decreased with somatostatin infusion and insulin-induced hypoglycemia. No other gut or pancreatic hormone levels in plasma were elevated. Plasma IRG was eluted by gel-filtration, mainly in the position of true glucagon (MW 3500) by antiserum 30K. The rash was markedly improved after infusion of amino acids. Computerized tomography (CT) scan and celiac angiography revealed a large pancreatic tumor with multiple liver and lymph node metastases. The pancreatic tumor was totally resected, and was identified as glucagonoma by immunohistochemical technique. Since the plasma IRG levels remained high after surgery, the patient received dimethyltriazenoimidazole carboxamide therapy. After several courses of this treatment, plasma IRG levels decreased to 1000 to 2000 pg/ml, and the hepatic metastases were remarkably diminished in size.

Adenoma, Islet Cell↗
PubMed1985

Comparison of somatostatin-28 and somatostatin-14 clearance by the perfused rat liver.

The hepatic clearances of somatostatin (SS)-28 and SS-14 by the perfused rat liver were compared, using a recirculating, plasma-free, erythrocyte-containing perfusion system. The disappearance rate constant, half time, clearance, and hepatic extraction ratio when 1.2 nM SS-28 was added to the perfusate were 0.0221 +/- 0.0051 min-1, 36.6 +/- 7.6 min, 0.34 +/- 0.08 mL/min, and 17.2 +/- 3.9%, respectively. The corresponding values obtained when SS-14 was added to the perfusate were 0.0405 +/- 0.0022 min-1, 17.3 +/- 1.0 min, 0.71 +/- 0.05 mL/min, and 35.4 +/- 2.6%, respectively. The differences between the SS-28 and SS-14 indices were all statistically significant. In addition, the perfusates with SS-28 added were eluted on Sephadex G-25 fine columns and somatostatinlike immunoreactivity (SLI) was determined. No SS-14 was found in perfusate containing SS-28 at both 5 and 30 min after the beginning of the perfusion. To investigate whether or not the liver plays an important role in the clearance of SS-28 or the conversion of SS-14 in vivo, the plasma disappearance of 2 micrograms SS-28 was compared in the whole rat and the functionally hepatectomized model. The half time of plasma SS-28 was 1.43 +/- 0.12 min in the whole rat, significantly shorter than the 2.20 +/- 0.14 min in the hepatectomized model. Gel filtration of plasma extract samples at 0.5 min after the SS-28 injection showed two major peaks of SLI: a first peak corresponding to SS-28 and a second peak coeluted in the position of SS-14 in both the whole rat and the hepatectomized model. At 4 min after the SS-28 injection, the first peak disappeared and only a small second peak was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1979

Theophylline: potentiation of arginine-induced somatostatin release from the isolated rat pancreas.

Somatostatin's release from the isolated rat pancreas was studied using a perfusion technique. Arginine at a concentration of 19 mM produced a biphasic increase in somatostatin release from the perfused rat pancreas. Both first and second phases of somatostatin's increase are significantly higher in the presence of 1 mM theophylline than in the absence of the drug. These results indicate the possible inclusion of the adenylate cyclase--cyclic AMP system in the regulatory mechanism of rat pancreatic somatostatin secretion.

Animals↗
PubMed1979

Somatostatin release from isolated perfused rat pancreas. Possible role of endogenous somatostatin on insulin release.

In order to elucidate the role of endogenous somatostatin in the control of insulin and glucagon secretion, glucagon- or insulin-induced somatostatin release from the isolated perfused rat pancreas was studied. Immunoreactive somatostatin was persistently released for 60 min in response to perfusion by 5.5 mM glucose at concentrations ranging between 10 and 15 pg/ml. The addition of glucagon (10(-8), 10(-7), and 10(-6) M) caused a dose-related increase of somatostatin release. In contrast, insulin release, especially its first phase, was suppressed when concentrations of glucagon were increased. The addition of insulin (10(-7) M and 10(-6) M) had no significant effect on somatostatin and glucagon release. These results raise the possibility that endogenous somatostatin and glucagon together regulate insulin secretion, suggesting a close interrelationship between insulin, glucagon, and somatostatin secretion within the islet.

Animals↗