Journal of the Japan Diabetes Society
Online ISSN : 1881-588X
Print ISSN : 0021-437X
ISSN-L : 0021-437X
Volume 31, Issue 6
Displaying 1-11 of 11 articles from this issue
  • Koji Kuboki
    1988 Volume 31 Issue 6 Pages 457-462
    Published: June 30, 1988
    Released on J-STAGE: August 10, 2011
    JOURNAL FREE ACCESS
    To elucidate the relationship between the 24-hr urinary excretion rate of fibronectin degradation products (24-hr U-FnDP) and intraglomerular thrombin generation in diabetic nephropathy, 24-hr U-FnDP, 24-hr urinary protein (24-hr U-), and the renal venoarterial difference in soluble fibrin monomer complexes (V-A·SFMC) were determined in 16 iabetic patients. Moreover, renal biopsy was performed in 7 diabetics with various degrees of 24-hr U-P to clarify the interaction of 24-hr U-FnDP with diffuse diabetic glomerular lesions.
    V-A·ESFMC was elevated roportionally (r=0.84, p<0.001) to the increase in 24-hr U-FnDP. 24-hr U-P also correlated positively (r=0.69, p<0.005) with V-A·SFMC. The progression of diffuse diabetic glomerular lesions was closely related to the ncrease in 24-hr U-FnDP and 24-hr U-P.
    It was concluded that 24-hr U-FnDP as well as 24-hr U-P might reflect the degree of intraglomerular thrombin generation and extent of diffuse diabetic glomerular lesions, while 24-hr U-FnDP would e a more suitable parameter of the development of diabetic nephropathy, because it has been reported that 24-hr U-FnDP is derived from glomeruli.
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  • T. Maruyama, T. Yanagawa, I. Takei, Y. Asaba, K. Kataoka, T. Saruta, T ...
    1988 Volume 31 Issue 6 Pages 463-469
    Published: June 30, 1988
    Released on J-STAGE: August 10, 2011
    JOURNAL FREE ACCESS
    Similar to the case of insulin-dependent diabetes mellitus (IDDM) in man, diabetes in nonobese diabetic (NOD) mice and that induced by multiple injections of low-dose streptozotocin (SZ) develops in conjunction with insulitis. We have analyzed whether the development of hyperglycemia in low-dose SZ-injected mice can be prevented by administration of the streptococcal preparation, OK-432, which has been reported to inhibit the development of Type 1 diabetes in NOD mice. Eightto ten-week-old male CD-1 mice were given SZ (30 or 40mg/kg body weight) on five consecutive days (day 0-4) and in addition, OK-432 or saline was injected intraperitoneally on days-5, 0, 7 and 14. The mice which received 40mg/kg of SZ became hyperglycemic and the mean blood glucose level was higher in OK-432-injected mice than in saline-injected controls. In the mice receiving 30mg/kg of SZ, 50% of OK-432-injected mice developed hyperglycemia, but saline-injected mice did not develop diabetes within the experimental period. Histological examination showed marked mononuclear cell infiltration of the islets in OK-432-injected mice compared with saline-injected controls. These results suggest that immunomodulators such as OK-432 may, in some cases, enhance islet cell destruction and exacerbate Type 1 diabetes in man.
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  • Reiko Kawahara, Masayo Yoshino, Teiko Amemiya, Tomonori Komori, Yukima ...
    1988 Volume 31 Issue 6 Pages 471-476
    Published: June 30, 1988
    Released on J-STAGE: August 10, 2011
    JOURNAL FREE ACCESS
    The frequency of hemoglobin F (HbF) persistece in 5, 167 diabetic patients was compared with that in 82 normal healthy controls.
    The results were as follows:
    1) 1, 023 diabetic patients (19.8%) had concentrations of HbF from 0.5% to 0.9% of the totalhemoglobin.
    197 diabetics (3.8%) had HbF from 1% to 1.9% of the total hemoglobin.
    45 diabetics (0.9%) had HbF from 2% to 2.9% of the total hemoglobin.
    45 diabetics (0.9%) had HbF from 3% to 6.9% of the total hemoglobin.
    None of these frequencies were significantly different from those in normal control subjects.
    2) Frequency of HbF persistence was higher in women, especially pregnnt women, than in men.
    3) Six of the 90 diabetic patients with HbF persistence above 2% had hyperthyroidism or hypothyroidism in their past history.
    4) There was no relationship between HbF and diabetic retinopthy or albuminuria.
    5) There was a strong correlation between HbF and HbA1-HbA1c (r=0.96), and also a significant correlation between HbF and HbA1 (r=0.55).
    We conclde that 25.4% of the diabetic patients had HbF levels greater than 0.5%, therefore, if there is a discrepancy between HbA1 and HbA1c, HbF persistence in the patient's sera might be considered.
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  • Kunio Yamanouchi, Osamu Shikata, Kiwami Chikada, Takashi Shinozaki, Hi ...
    1988 Volume 31 Issue 6 Pages 477-482
    Published: June 30, 1988
    Released on J-STAGE: August 10, 2011
    JOURNAL FREE ACCESS
    The present study was performed to assess the clinical usefulness of serum fructosamine as an indicator of blood glucose control. Diabetic outpatients with stable blood glucose levels were examined for correlations between hemoglobin A1 (HbA1), fasting and postprandial blood glucose and fructosamine levels. In addition, 11 poorly-controlled diabetic inpatients who were being brought under control with strict conventional insulin therapy were examined to determine whether parallel changes occur in fructosamine and blood glucose levels. Fructosamine showed the best correlaton with HbA1, in diabetic outpatients with stable blood glucose levels (p<0.05) In poorly controlled diabetic inpatients, one week after insulin treatment, fructosamine had decreased significantly concomitant with the decrease in mean blood or urinary glucose values (p<0.01). Return of fructosamine to stable, near-normal levels was slower (2 weeks) than stabilization of blood glucose levels. A significant decrease in fructosamine, but not in HbA1, occurred after four weeks of treatment of poorly controlled diabetics. Fructosamine levels were stable, i.e. showed no transient increase, in response to the normal increase in postprandial blood glucose in well-controlled diabetic patients. These results indicate that the serum fructosamine level is a useful indicator for the averae blood glucose level from the preceding several days to about 2 weeks.
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  • An Age-, Sex-and Institute-matched Study
    Ken Horigome, Yukihiro Kai, Fuminobu Okuguchi, Masaei Kakizaki, Kenich ...
    1988 Volume 31 Issue 6 Pages 483-490
    Published: June 30, 1988
    Released on J-STAGE: August 10, 2011
    JOURNAL FREE ACCESS
    A cross-sectional study of retinopathy and ischemic changes in ECG (IC) was performed on 332 male and 306 female adult diabetics from 6 institutes. The prevalence rate of IC was higher in females than in males. The patients with retinopathy or with IC were compared with age-, sexand institute-matched control diabetics. Duration of diabetes, hypertension and low HDL-cholesterol were closely related to retinopathy, especially to proliferative retinopathy in both sexes. Triglyceride was on additional factor in females. With regard to IC, systolic blood pressure was the only correlate in both sexes. In females, triglyceride was an additional factor. No correlation of total cholesterol, HDL-cholesterol or cigarette smoking with IC was seen. The pathogeneses of retinopathy and IC were suggested to be independent of each other, although the two complications had some common risk factors such as hypertension or triglyceride.
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  • Comparative Study of Normal and Diabetic Live
    Hiromi Matsumae, Nigishi Hotta, Ryuzo Kito, Jiro Nakamura, Fumihiko Sa ...
    1988 Volume 31 Issue 6 Pages 491-498
    Published: June 30, 1988
    Released on J-STAGE: August 10, 2011
    JOURNAL FREE ACCESS
    It is well established that the plasma level of oxytocin as well as of vasopressin is markedly elevated in the hypovolemic state. However, it remains to be established whether oxytocin has any role in the severe diabetic state accompanied by hypovolemia. In the present study, the effects of oxytocin on liver metabolism in the presence of 10mM L-alanine were observed in isolated perfused livers from 20-hour-fasted normal and streptozotocin-induced diabetic rats. Oxytocin had a direct effet on the stimulation of gluconeogenesis and ketogenesis. These increases due to oxytocin (1×10-7M) were similar to those due to vasopressin (0.8mU/ml) and glucagon (2.86×10-7M). Insulinat the physiological concentration suppressed the oxytocin-induced gluconeogenesis and ketogenesis, and this inhibition was more marked in the normal state than in the diabetic state. These results strongly suggest that oxytocin plays a role in the aggravation of metabolic disorders in the severe diabetic state.
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  • Evidence for Familial Occurrence of Post-binding Defect in Insulin Action
    Shinobu Kumakura, Yoshikazu Sakamoto, Yasuhiko Iwamoto, Ayako Matsuda, ...
    1988 Volume 31 Issue 6 Pages 499-504
    Published: June 30, 1988
    Released on J-STAGE: August 10, 2011
    JOURNAL FREE ACCESS
    We report a case of familial insulin resistance due to a post-binding defect in insulin action, the type C syndrome of insulin receptor diseases. The patient was a 16-year-old girl with acanthosis nigricans and hyperinsulinemia. Hirsutism and polycystic ovary syndrome were absent. She had normal glucose tolerance as shown by a 100g oral glucose tolerance test, but her plasma insulin level was 40μU/ml at fasting and was as high as 746μU/ml during OGTT. She showed a blunted hypoglycemic response to an injection of 0.1U/kg exogenous insulin, indicating the presence of insulin resistance. Anti-insulin antibodies and anti-insulin receptor antibodies were not detected. Insulinbinding to erythrocytes was nearly normal. There was no proinsulin-like component in plasma by gel filtration with Biogel P-30. Plasma insulin was purified by affinity chromatography using anti-insulin serum. Only one peak of normal human insulin was detected by HPLC analysis. The patient's insulin competed normally with 125I-insulin for binding to insulin receptors from plasma membrane of guinea pig kidney, and exhibited a normal biological potency for stimulation of glucose oxidation of rat adipocytes. Her mother and two brothers also had hyperinsulinemia at fasting and after oral glucose load. The findings indicate that the patient's insulin resistance was due to a postbinding defect that was probably genetic in nature.
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  • Yasushi Tanaka, Masatoshi Nagao, Toshiji Nishio, Etsu Hashida, Atsunor ...
    1988 Volume 31 Issue 6 Pages 505-511
    Published: June 30, 1988
    Released on J-STAGE: August 10, 2011
    JOURNAL FREE ACCESS
    We report a case of diabetic ketoacidosis induced by acute pancreatitis in the course of noninsulin-dependent diabetes mellitus (NIDDM).
    The patient was a 17-year-old man, who was calssified as having NIDDM with remarkableobesity (obesity index 1.41) and poor control of diabetes (HbA1c 13.4%).
    On June 17, 1987, he was admitted to our hospital because of consciousness loss due to diabetic ketoacidosis accompanied by acute pancreatitis. By continuous intravenous insulin infusion, the blood glucose level was decreased from 950 to 271 mg/dl within 7 hours after admission. However, in spite of continuous intravenous insulin infusion (120-280 U/day), the blood glucose level fluctuated markedly between 80 and 600 mg/dl with a remarkably low level of serum IRI (9.5μU/ml). Following intravenous infusion of gabexate mesilate (1, 500 mg/day) for the treatment of disseminted intravascular coagulation (DIC), the daily insulin requirement was decreased gradually, and the level of serum IRI reached 29.1μU/ml by even low-dose insulin infusion (106 U/day). Unfortunately, he died of DIC, multiple organ failure and hypernatremia on June 29.
    The present case demonstrated the following features;
    (1) Diabetic ketoacidosis was induced by acute pancreatitis in NIDDM showing poor metabolic control.
    (2) The complication of acute pancreatitis in NIDDM induced not only deterioration of metabolic control but also poor life prognosis.
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  • Effect of Perfusate Glucose Concentration
    Tadasu Ikeda, Mamoru Honda, Tatsuo Takeuchi, Osamu Mokuda, Masato Tomi ...
    1988 Volume 31 Issue 6 Pages 513-515
    Published: June 30, 1988
    Released on J-STAGE: August 10, 2011
    JOURNAL FREE ACCESS
    To determine the direct effect of arterial glucose concentration on urinary excretion of N-acetyl-β-D-glucosaminidase (NAG), NAG activity was measured in the urine from rat kidneys vascularly perfused for 40min with a synthetic medium containing 5.5mmol of glucose, 16.7mmol of glucose, or 5.5mmol glucose and 11mmol of mannitol. Urinary NAG activity in the kidney perfused with 16.7mmol of glucose (2.9±1.3mU/40min, mean±SD) was significantly greater than that (0.5±0.1mU/40min or 0.6±0.2mU/40min) perfused with 5.5mmol of glucose or 5.5mmol of glucose and 11mmol of mannitol, respectively.
    These results suggest that urinary NAG excretion is strongly influenced by arterial blood glucose concentration.
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  • 1988 Volume 31 Issue 6 Pages 517-528
    Published: June 30, 1988
    Released on J-STAGE: August 10, 2011
    JOURNAL FREE ACCESS
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  • 1988 Volume 31 Issue 6 Pages 529-543
    Published: June 30, 1988
    Released on J-STAGE: August 10, 2011
    JOURNAL FREE ACCESS
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