All issues
Volume 37, Issue 4
Displaying 1-10 of 10 articles from this issue
- |<
- <
- 1
- >
- >|
-
Hiroyuki Ishii, Hisaya Tada1994 Volume 37 Issue 4 Pages 247-253
Published: April 30, 1994
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSThis study was performed to elucidate the effect of high glucose concentrations (HGs) on the proliferation, cytotoxicity, attachment and spreading of cultured mesangial cells, and also to examine whether hypertonicity and the enhanced polyol pathway contribute to these abnormalities.
At HGs, both cell count and [3H]-thymidine uptake were lower than at low glucose concentrations (LGs). A high mannitol concentration (HM) had a similar effect with less effect on [3H] thymidine uptake than HG. Reduced [3H]-thymidine uptake, i.e., decreased proliferation induced by HGs was not restored by epalrestat. On the other hand, increased [51Cr]-release and inhibition of cell attachment and spreading were observed at HGs, but not at HMs. These abnormalities were prevented by epalrestat.
In conclusion, HG brought about decreased proliferation, increased cytotoxicity and impaired attachment and spreading of mesangial cells. It is assumed that the alterations in cytotoxicity, cell attachment and spreading under HG conditions are linked to the enhanced polyol pathway.View full abstractDownload PDF (1001K) -
Masami Nemoto, Yutaka Mori, Junichi Yokoyama, Masahiko Nishimura, Yosh ...1994 Volume 37 Issue 4 Pages 255-259
Published: April 30, 1994
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSThe Long Evans Tokushima lean (LETL) rat is a newly developed animal model of human type I diabetes mellitus, and we previously reported that Cyclophosphamide (CY) promoted the onset of diabetes in this rat strain. In the present study, we examined the preventive effects of large-dose Nicotinamide (NA) administration on CY-induced diabetes in LETL rats. Seventy-seven LETL rats were randomly divided into three groups; 25 were maintained as a control group to which saline was administered by injection, 33 were given two intraperitoneal injections (100mg/kg each) of CY, and 19 received daily subcutaneous NA (500mg/kg body weight) injections after CY administration. A non diabetic strain, LETO (n=11) was also injected with CY. After 10 weeks, histological examination of the pancreas was performed. The cumulative incidences of diabetes were 8.0%, 36.4%, an 15.8% in control, CY treated, and CY and NA-treated LETL rats, respectively. No LETO rats developed diabetes. The severity of insulitis was graded as 0 to 3 histologically. The mean severities of insulitis were O, 0.05±0.019, and 0.31±0.61 in control, CY-treated, and CY and NA treated non diabetic LETL rats, respectively. In conclusion, large-dose NA treatment prevented the development of CY induced diabetes in LETL rats although, histologically, insulitis was not suppressed.View full abstractDownload PDF (740K) -
Takashi Kudo, Masaaki Kameyama1994 Volume 37 Issue 4 Pages 261-269
Published: April 30, 1994
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSIn order to elucidate the relationship between hyperglycemia and both the concentration and solubility of circulating plasma soluble fibrin monomer complexes (SFMC), in the course of acute myocardial infarction (AMI), 15 cases of AMI with various degrees of glucose intolerance were studied. Furthermore, the effect of a high glucose concentration on the fibrin fiber diameter was observed experimentally.In the Group I patients (comprised of 8 impaired glucose tolerance (IGT) cases among 10 patients, Fructosamine (FRA)≤285μmol/l), the elevated SFMC and Fbg concentrations had decreased to nearly the same level as the pretreatment value by the 14 th hospital day. On the other hand, in the Group II patients (comprised of 5 diabetics, FRA>285μmol/l), the high SFMC level became more elevated and the increased Fbg concentration had not decreased by the 14 th hospital day.Plasma Fn levels of both groups did not show a significant increase over this period.The ratio of Fn to fibrin (ogen) obtained as a marker of SFMC solubility had increased markedly by the 14 th hospital day, and exhibited a mirror image when compared with the change in SFMC level.In contrast, Group II showed a tendency for this ratio to decrease.The fibrin fiber diameter formed from glycated Fbg and Fn was enlarged.
These results suggest that persistent hyperglycemia may induce prolonged intravascular thrombin generation and the formation of SFMC with low solubility.As this seems to be an unfavorable condition for patients with AMI, it is concluded that glycemic control is particularly important for diabetic patients with AMI.View full abstractDownload PDF (3002K) -
Yoshifumi Takagi, Atsunori Kashiwagi, Hiroshi Maegawa, Yukio Shigeta1994 Volume 37 Issue 4 Pages 271-278
Published: April 30, 1994
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSHyperinsulinemia is known as one of the risk factors for atherosclerosis. However, its effects at physiological concentrations on vascular smooth muscle cells (VSMCs) are still controversial. Therefore, we examined whether a specific signal transduction pathway for insulin exists and if so, whether it can be desensitized by continuous exposure to insulin. Specific [125I] insulin binding was found on VSMCs and was inhibited by 50% with 330pM unlabeled insulin, which was 100 times less than the inhibition produced by unlabeled IGF-I. Autophosphorylation of insulin receptor (IR) and S6 kinase activity significantly increased at more than 0.17 nM (24μU/ml) and 1 nM (144μU/ml) insulin, respectively. Following continuous insulin treatment (10 nM, 12 hr), [125I] insulin binding decreased by 39% with no change in [125I] IGF-I binding. Similarly, this treatment reduced the insulin-induced S6 kinase activity by 67% without reducing that induced by IGF-I. These results indicate that some insulin effects on VSMCs are mediated through IR and that they are desensitized by continuous exposure to insulin in vitro.View full abstractDownload PDF (2570K) -
Immunohistochemical Study on Synaptic Regions of Rat HippocampusTohru Kawabata, Hitoshi Yasuda, Yukio Shigeta1994 Volume 37 Issue 4 Pages 279-288
Published: April 30, 1994
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSIn order to clarify the pathogenesis and evolutional mechanism of hypoglycemic neuronal death, we performed an immunohistochemical study of the rat hippocampus after severe hypoglycemia (isoelectric EEG for 30 min) by the ABC method using monoclonal antibodies against MAP2 (postsynaptic dendritic protein), synaptophysin (presynaptic protein) and GAP43 (presynaptic protein associated with axonal growth, synaptogenesis and neurotransmitter release).
At 30 min after hypoglycemia, MAP2 immunoreactivity was transiently decreased in the lateral CA1 region in which pyramidal cells appeared unchanged. During the period from 2 hours to 7 days after hypoglycemia, neuronal necrosis first appeared in granular cells of the dentate crest and gradually extended from the subiculum and CA1 to CA2 with decreasing MAP2 and increasing GAP 43 immunoreactivity. In the initial stage of this process, GAP 43 immunoreactivity was found in the inner molecular layer (presynaptic regions of granular cells) of the dentate gyms before the granular cells started to undergo necrosis. The area positively stained with GAP 43 gradually extended and the intensity of its immunoreactivity was maximal at day 7, when immunoreactivity was found even around necrotic neurons. The immunoreactivity of synaptophysin after hypoglycemia was almost identical to that of GAP 43 in distribution and temporal profile, although the latter exceeded the former in the intensity of the immunoreactivity.
These results suggest that the evolutional mechanism of hypoglycemic brain damage differs from that of ischemic brain damage and that GAP 43 may play an important role in the development of hypoglycemic neuronal death and in synaptic regeneration after neuronal death.View full abstractDownload PDF (8284K) -
Mayumi Osawa, Asako Sato, Yasuko Takano, Sumiko Hasumi, Yasue Omori1994 Volume 37 Issue 4 Pages 289-293
Published: April 30, 1994
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSA 37 year old man was admitted to our hospital on January 10th, 1992, because of nausea, vomiting and body weight loss.He was obese but otherwise well until December, 1991, when he developed thirst, polydipsia and polyuria.Nausea and vomiting appeared after the development of gingivitis.Over eating and excessive alcohol intake resulted in severe anorexia and body weight loss.On admission he was alert although laboratory findings revealed 635mg/dl of blood glucose and 9700μmol/l of 3 beta hydroxybutyrate.Marked hypochloremia of 77mEq/l was also present and the arterial blood gas revealed an alkaline pH of 7.571, PaCO2 of 14.1mmHg and bicarbonate of 13.0mmol/l.Taken together, these data indicated that he was in a state of hypochloremic alkalosis and diabetic ketoacidosis compensated for by hyperventilation. Such cases are rare and interesting from the viewpoint of acid base equilibrium.View full abstractDownload PDF (614K) -
Kensou Ohsawa, Nobuhiko Koike, Toshinari Takamura, Yukihiro Nagai, Ken ...1994 Volume 37 Issue 4 Pages 295-300
Published: April 30, 1994
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSWe report three cases of non-insulin-dependent diabetes mellitus who experienced frequent attacks of hypoglycemia after administration of bezafibrate for hyperlipideniia.Although they had been treated with glibenclamide, glycemic control was unsatisfactory in all three, and one patient was considered a sulfonylurea failure.Several days after the addition of bezafibrate, blood glucose levels decreased, even to the point of hypoglycemia.Therefore, 2.5mg of glibenclamide was changed to500mg of tolbutamide in case 1, 6.25mg of glibenclamide was reduced to 2.5mg in case 2, and 10mg of glibenclamide and 100mg of buformin were stopped in case 3.These patients subsequently maintained good glycemic control without hypoglycemia.
As all of these cases were elderly and two of them had mild renal dysfunction, clearances of glibenclamide and bezafibrate were assumed to be decreased.Therefore, it was suggested that the hypoglycemic effects of glibenclamide and bezafibrate were potentiated due to elevated plasma levels of these drugs and exaggerated drug-interactions.View full abstractDownload PDF (779K) -
Keiichiro Tanigawa, Satoshi Ohguni, Yuzuru Kato1994 Volume 37 Issue 4 Pages 301-306
Published: April 30, 1994
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSWe studied the metabolic effects of a new oral antidiabetic agent, CS-045 (400mg/day), in a 39-year old woman with glycogen storage disease type Ia complicated by diabetes mellitus. During the six month period before treatment with CS-045, mean HbA1c levels were 8.4%. Ten weeks after the start of CS-045 treatment, blood glucose and HbA1c levels were showing tendencies to decrease. Six months after the start of CS-045 treatment, HbA1c showed a definite decrease. Five months after the start of CS-045 treatment, a 75 g oral glucose tolerance test showed decreased blood sugar levels and increased secretion of C-peptide as compared with values obtained on the previous test before treatment. The metabolic clearance rate of glucose determined by euglycemic glucose clamp was decreased before treatment, suggesting the presence of insulin resistance. CS-045 was effective in ameliorating this pathological condition.View full abstractDownload PDF (888K) -
Evaluated by Doppler Echography and Laser Blood FlowmetryHirohito Sone, Yukichi Okuda, Masakazu Mizutani, Yukari Asakura, Michi ...1994 Volume 37 Issue 4 Pages 307-310
Published: April 30, 1994
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSIbudilast (3-isobutyryl-2-isopropylpyrazolo-[1.5a] pyridine) is a prostacyclin mediated vasodilator and anti-platelet agent that has a relatively long duration of action and is orally active. Non-insulin dependent diabetic patients were studied to evaluate the effects of ibudilast on hemodynamic changes in the circulation by two dimensional Doppler echography and laser blood flowmetry. Before and 1 h after administration of ibudilast (10 mg) or elastase (1800 U), the cross-sectional area (Area) of the dorsal pedis artery and its Blood Flow Index (BFI), calculated from maximum flow velocity and Area, were determined. Dermal microcirculatory blood volume (MCBV) was also measured with the laser blood flowmeter. In the ibudilast group, the Area was significantly increased from 2.72±0.32 to 3.21±0.35mm2 (Mean±SE, p<0.05). The BFI was also siginificantly increased from 28.3±3.7 to 37.0±5.2 (p<0.01). In the ibudilast group, MCBV was also significantly increased from 3.82±0.70 to 4.96±0.71 ml/min/100g tissue (p<0.01). No significant changes were observed in the data of the elastase group, and no side effects were observed in any of the patients in either of group. The results of this study suggest that ibudilast may be useful in ameliorating diabetic macro-and microangiopathy of the lower limbs.View full abstractDownload PDF (446K) -
Masayuki Inouye, Akimitsu Tsutou, Kyoya Narutaki1994 Volume 37 Issue 4 Pages 311-315
Published: April 30, 1994
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSExtracted lipids from erythrocyte membranes were analyzed by gas chromatographic mass spectrometry.Hydroxy stearic acid and hydroxy lignoceric acid were not detected in healthy subjects but were present in diabetic patients, using ion chromatography.Findings were confirmed by mass spectrometry.These analytical findings suggest that 1) peroxidation of poly-unsaturated fatty acids occurs due to the suppression of superoxide dismutase activity in diabetic erythrocytes, 2) from a physiochemical point of view, these hydroxy fatty acids might be associated with reduced fluidity of the erythrocyte membranes in diabetics, and 3) ion chromatography is useful for detecting hydroxy fatty acids of erythrocyte membranes.View full abstractDownload PDF (448K)
- |<
- <
- 1
- >
- >|