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Volume 35, Issue 9
Displaying 1-13 of 13 articles from this issue
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[in Japanese]1992 Volume 35 Issue 9 Pages 711-712
Published: September 30, 1992
Released on J-STAGE: March 02, 2011
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[in Japanese]1992 Volume 35 Issue 9 Pages 713-718
Published: September 30, 1992
Released on J-STAGE: March 02, 2011
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[in Japanese], [in Japanese]1992 Volume 35 Issue 9 Pages 719-721
Published: September 30, 1992
Released on J-STAGE: March 02, 2011
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[in Japanese]1992 Volume 35 Issue 9 Pages 723-726
Published: September 30, 1992
Released on J-STAGE: March 02, 2011
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[in Japanese]1992 Volume 35 Issue 9 Pages 727-729
Published: September 30, 1992
Released on J-STAGE: March 02, 2011
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Hisayoshi Oka, Soichiro Mochio, Kenichi Sato1992 Volume 35 Issue 9 Pages 731-738
Published: September 30, 1992
Released on J-STAGE: August 04, 2011
JOURNAL FREE ACCESSWe evaluated autonomic nervous system dysfunction in diabetic patients by an objective and quantitative sympathetic function test using the QT interval. We constructed a regression line of QT interval with respect to R-R interval in 602 healthy controls to obtain a QT interval independent of R-R interval. We also measured ΔQT, which was the difference between the measured and theoretical QT intervals obtained from the regession line in healthy controls. The ΔQT was prolonged by propranolol and should thus reflect sympathetic nervous function. The QT intervals of 59 diabetic patients (NIDDM) were measured. The ΔQT of those patients was compared with that of the 59 age-matched controls. We also examined the relationship between the clinical features of diabetes mellitus and the ΔQT. The regression line was QT (msec)=0.143×R-R (msec)+243. The ΔQT of diabetic patients (17 msec) was significantly greater than that of the 59 age-matched healthy controls (7 msec), though it was not related to the duration of diabetes, diabetic control, or the presence of retinopathy or proteinuria. However, the ΔQT of patients with delayed nerve conduction velocity (22 msec) or orthostatic hypotension (30 msec) was significantly greater than that without these. Significant correlations were found between the ΔQT in diabetic patients and the Valsalva ratio, the Valsalva overshoot, or the plasma concentration of noradrenaline.ΔQT should be useful in the clinical evaluation of sympathetic nervous system dysfunction in diabetic patients.View full abstractDownload PDF (1256K) -
Masanori Iwanishi, Masashi Kobayashi, Yukio Shigeta1992 Volume 35 Issue 9 Pages 739-745
Published: September 30, 1992
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSA new oral agent, 5-[4-[2 (5-ethyl 12-pyridyl) ethoxy]-benzoyl]-2, 4-thiazo lidinedione pioglitazone, has been developed for treatment of NIDDM. We examined its offectiveness in high fat-fed rats with insulin resistance. Administration of the agent (10mg/day/kg) for two weeks decreased hyperlipidemia and hyperinsulinemia, indicating that the agent increases insulin sensitivity in vivo in high fat-fed rast. To clarify the mechanism by which the drug increases insulin sensitivity, we examined the insulin binding and kinase activity of insulin receptors form muscles of rats fed with either a high fat or non-high fat diet. Pioglitazone treatment did not change insulin binding in the high fat-fed rats, but it increased insulin-stimulated autophosphorylation of insulin receptors to the level of the control group. Although kinase activity toward an exogenous substrate, poly Glu4Tyr1, tended to increase to the level of the control animals, The difference was not significant. These results suggest that pioglitazone increases insulin sensitivity in part by activating autophosphorylation of the receptors and that the drug appears to be a useful one, with a new mode of action for treating the insulin resistance in NIDDM.View full abstractDownload PDF (2095K) -
Cytoplasmic Free Ca2+ and Insulin SecretionNobuyuki Takasu, Ichiro Komiya, Yoshitaka Nagasawa, Takayuki Asawa, Ta ...1992 Volume 35 Issue 9 Pages 747-753
Published: September 30, 1992
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSGlucose-stimulated insulin release is believed to be mediated by an increase in cytoplasmic free Ca2+ ([Ca2+] i). Previous exposure to high glucose concentrations decreases the subsequent glucose stimulated insulin release. To reveal the mechanism of this, we studied the effects of previous exposure to high glucose concentrations on glucose-stimulated insulin release and on glucose-stimulated [Ca2+] i response, using rat pancreatic islets.
Glucose stimulated insulin release from pancreatic islets in perfusion and perifusion systems. Previous exposure to high glucose concentrations in rat pancreatic islets in vivo and in vitro decreased the subsequent glucose-stimulated insulin release. We also studied the glucose-stimulated [Ca2+] i response, using fura-2. Glucose induced [Ca2+] i response. Previous exposure to high glucose concentrations also decreased this glucose-stimulated [Ca2+] i response. Previous exposure to high glucose concentrations decreased both the glucose-stimulated [Ca2+] i response and insulin release, suggesting that impaired glucose-stimulated [Ca2+] i response may be associated with impaired glucose-stimulated insulin release.View full abstractDownload PDF (914K) -
Tomio Nakayama, Kazumasa Chikamori, Toshinao Yamano, Kozo Hashimoto, F ...1992 Volume 35 Issue 9 Pages 755-760
Published: September 30, 1992
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSThe pancreas of 5 patients with IDDM in remission (group A), 12 with IDDM not in remission (group B), 120 with NIDDM (group C), and 100 healthy controls group were scanned by ultrasound to investigate the relationship between pancereatic functions and morphology. The P value (an area including the pancereatic head, body, and tail) was determined in the transverse or oblique plane parallel to the splenic vein. The Q value was calculated by dividing the P value by the body surface area. The values for the aforementioned 4 groups were 7.9±1.2, 4.7±1.2, 6.8±1.9, and 8.9±1.5cm2/m2 (mean+SD), respectively. The Q value for group A was significantly greater than that for group B (P<0.01). The serum trypsin level of group A was significantly higher than that p<0.01 for group B (P<0.01). As a prospective study, time course of Q value in 3 IDDM with remission (Group A'), and 3 IDDM without remission (Group B') were followed up. Pancreatic atrophy and pancreatic exocrine dysfunctions developed rapidly after onset in the Group B' but not in the Group A'. No significant differences were noted in pancreatic endocrine function, presence or absence of ICA or ICSA, and HLA or HbA1c values of the group A and group B. It was concluded that the Q value and serum immunoreactive trypsin level may be good indicators for remission in IDDM.View full abstractDownload PDF (998K) -
Michiyo Seno, Hisao Nishida, Tomohiko Taminato, Kinsuke Tsuda, Hiroo I ...1992 Volume 35 Issue 9 Pages 761-766
Published: September 30, 1992
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSWe investigated the interrelationship between blood pressure and glucose tolerance in 6250 subjects from the Multiphasic Health Testing and Service Section of Kampo Medical Center. All subjects underwent a standard 75 g oral glucose tolerance test. Blood pressure was measured and classified into groups based on WHO criteria. Plasma IRI was measured in 576 subjects.
The prevalence of diabetes mellitus in the hypertensive group was 18.4%, significantly higher than the 7.4% in the normal group. The 1-hour postload plasma glucose, and 2-hour plasma glucose levels in the hypertensive group were significantly higher than those of the normal group in both obese and non-obese subjects.
The fasting plasma IRI concentration correlated significantly with both systolic and diastolic blood pressure in subjects with normal glucose tolerance. The fasting plasma IRI levels were significantly higher in the hypertensive group than in the normal group in both obese and non-obese subjects. Furthermore, in subjects with normal glucose tolerance, the fasting plasma IRI concentration was also significantly higher in the hypertensive group than in the normotensive group.
These results suggest that insulin resistance which expresses itself as compensatory hyperinsulinemia may be the common factor in pathogenetic interactions between high blood pressure and glucose intolerance, independent of obesity.View full abstractDownload PDF (1035K) -
Special Reference to Coronary Risk Factors and Blood Glucose ControlYoshimori Minemawari, Nagisa Hanawa, Teruaki Mita, Masaomi Motoe, Hiro ...1992 Volume 35 Issue 9 Pages 767-772
Published: September 30, 1992
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSTo elucidate the pathogenetic significance of coronary artery disease in diabetes mellitus, the effects of coronary risk factors on the severity of coronary angiographic findings were studied in 47 diabetics and 71 non-diabetics with significant coronary artery disease exceeding 75% stenosis. In the 47 diabetics the effects of methods of therapy, presence of diabetic microangiopathic complications, and control of blood glucose were also studied. In studying the effects of coronary risk factors other than diabetes mellitus, no significant difference between diabetic and non-diabetic patient groups was found. Moreover, there was no significant difference between respective intra-groups. In the studies of only diabetics, regarding the effects of methods of therapy, presence of diabetic microangiopathic complications and control of blood glucose, there were no significant differences among diet, oral hypoglycemics and insulin therapy, nor between patients with and without diabetic microangiopathic complication. But there was a significant correlation between the severity of coronary angiographic finding and HbA1c (r=0.655, p<0.001).
In conclusion, while this study does not definitively rule out the importance of coronary risk factors other than diabetes mellitus, it does suggest that abnormal glucose metabolism directly induces diabetic microangiopathy, and that it accelerates coronary artery disease in the setting ofmacroangiopathy in diabetes mellitus.View full abstractDownload PDF (677K) -
Kumiko Kojima, Ryoichi Okiyama, Masayuki Ohta, Yasuhiko Ishige, Miho A ...1992 Volume 35 Issue 9 Pages 773-777
Published: September 30, 1992
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSWe report a patient with diabetes mellitus who presented an isolated oculomotor nerve palsy due to cerebral infarction. The patient was a 61-year-old male with a six-year duration of non-insulin-dependent diabetes mellitus and hypertension. He complained of double vision and subsequent left ptosis. On admission, left oculomotor nerve palsy with pupil involvement was observed. No other neurological deficit, such as ataxia, was evident. On MRI, a mid-brain infarct considered to be responsible for the symptoms was demonstrated. A CT scan did not reveal the lesion.
It has been generally accepted that diabetic oculomotor palsy is caused by ischemia of the peripheral portion of the nerve. However, a small mid-brain lesion, as in the present case, can cause an isolated ipsilateral oculomotor palsy. It is possible that small mid-brain infarcts may have been misdiagnosed in the past, especially when there was coexistent diabetes mellitus. For the accurate diagnosis and proper management of such cases, MRI appears to be quite useful.View full abstractDownload PDF (2864K) -
Jinya Suzuki, Koji Oida, Akihiko Shimada, Sadao Takahashi, Hajime Maed ...1992 Volume 35 Issue 9 Pages 779-785
Published: September 30, 1992
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSA 25-year-old man who presented with eruptive xanthomas, hyperglycemia and hyperlipidemia was admitted to our hospital. Fasting plasma glucose, plasma total cholesterol (T-Ch) and plasma triglyceride (TG) were 286mg/dl, 420mg/dl and 1960mg/dl, respectively. Eruptive xanthomas were observed on his elbows, knees and hip. We diagnosed him as having insulin-dependent diabetes mellitus complicated with type V hyperlipoproteinemia; chylomicronemia syndrome. Following the reduction of plasma glucose level by conventional insulin therapy, T-Ch and TG were decreased and eruptive xanthomas diminished rapidly. Finally his plasma glucose level was normalized without insulin therapy. T-Ch decreased to normal range, but TG was still around 200mg/dl showing mild type IV hyperlipoproteinemia. His mother, who suffered from non-insulin-dependent diabetes mellitus, and his pregnant elder sister showed moderate hypertriglyceridemia. The Apo E isoform of the subject was E3/E3. His lipoprotein lipase (LPL) mass content was reduced to the level of heterozygous LPL deficiency even after normalization of plasma glucose. His parents' LPL mass contents were within normal range.
Although we could not definitely diagnose this subject as having heterozygous LPL deficiency, the insulin-dependent diabetic state seemed to have augmented the genetic hypertriglyceridemia.View full abstractDownload PDF (3758K)
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