Journal of the Japan Diabetes Society
Online ISSN : 1881-588X
Print ISSN : 0021-437X
ISSN-L : 0021-437X
Volume 31, Issue 12
Displaying 1-10 of 10 articles from this issue
  • [in Japanese]
    1988 Volume 31 Issue 12 Pages 887-888
    Published: December 30, 1988
    Released on J-STAGE: August 10, 2011
    JOURNAL FREE ACCESS
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  • D.E. McMillan
    1988 Volume 31 Issue 12 Pages 889-892
    Published: December 30, 1988
    Released on J-STAGE: August 10, 2011
    JOURNAL FREE ACCESS
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  • Torsten Deckert
    1988 Volume 31 Issue 12 Pages 893-896
    Published: December 30, 1988
    Released on J-STAGE: August 10, 2011
    JOURNAL FREE ACCESS
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  • A Follow-up Study for 6 Years
    Toshika Otani, Yuko Higami, Tadasu Kasahara, Hiroki Yokoyama, Kenshi Y ...
    1988 Volume 31 Issue 12 Pages 897-902
    Published: December 30, 1988
    Released on J-STAGE: August 10, 2011
    JOURNAL FREE ACCESS
    Two hundred thirty six patients with diabetes who had been diagnosed as diabetics under the age of 25, and referred to the Diabetes Center or the Department of Pediatrics of Tokyo Women's Medical College, were examined changes in incidence of retinopathy over a 6-year period. They consisted of 167 patients with (IDDM)(mean age of onset, 10.0±6.0 years; duration of diabetes, 15.1±6.1 years in 1986), and 69 with (NIDDM)(mean age of onset, 20.0±3.7 years; duration of diabetes, 15.3±0.9 years). Between 1980 and 1986, the incidence of retinopathy increased by 16.8% to 56.9% in patients with IDDM, but by only 4.4% to 56.5% in patients with NIDDM. When the duration was under 10 years, the incidence of retinopthy in NIDDM patients was higher than that in IDDM patients. The longer was the duration of diabetes, however, the more the incidence of retinopathy in IDDM patients increased.
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  • Takahiko Nakamura, Makoto Otsuki, Yoshinori Okabayashi, Masatoshi Fuji ...
    1988 Volume 31 Issue 12 Pages 903-908
    Published: December 30, 1988
    Released on J-STAGE: August 10, 2011
    JOURNAL FREE ACCESS
    Pancreatic B-cell function in liver cirrhosis was examined in rats. Experimental liver cirrhosis was induced by subcutaneous injection of 50% carbon tetrachloride of a dose of 2 ml/kg body weight twice a week for 16 weeks. Control rats received a similar dose of olive oil during the same period. The peripheral insulin level was higher in cirrhotic rats than in control rats. However, the insulin content of the cirrhotic rat pancreas was significantly lower than that in the control rat pancreas. Insulin secretion in response to both 16.7 mM glucose-and 100 pM cholecystokinin octapeptidestimulation from isolated perfused pancreata prepared from cirrhotic rats was only 60% of that from control rats. In contrast, there was no significant difference in arginine-stimulated insulin release between these two groups.
    These findings suggest that the peripheral insulin level was higher, whereas insulin release from the isolated perfused pancreas was lower in liver cirrhotic rats than in control rats. Moreover, there was a selective impairment of the stimulus-secretion mechanism of B cells in cirrhotic rats.
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  • Diabetic Nephropathy
    Yutaka Mori, Junichi Yokoyama, Masahiko Nishimura, Hideaki Kurata, Jun ...
    1988 Volume 31 Issue 12 Pages 909-915
    Published: December 30, 1988
    Released on J-STAGE: August 10, 2011
    JOURNAL FREE ACCESS
    We have recently reported a new diabetic strain of rat (WBN/Kob) with endo-exocrine pancreatic insufficiency. In this strain, insulin administration is usually not necessary for survival and the strain is suitable for long-term observation. In the present study, we examined the time course of urinary protein excretion, renal function and histological changes of the kidney in order to investigate the development of diabetic nephropathy.
    In male diabetic rats, 24-hour urinary total protein excretion began to increase at about 10 months of age and reached 25-300mg/24hr at 13 to 24 months of age. Electrophoretic analysis revealed that the urinary protein consisted of albumin. Under the light microscope, glomeruli with segmental or global increase in mesangeal areas were noted at 17 months of age, indicating development of marked glomerulosclerosis. Electron microscopic examination, revealed that the glomerular basement membrane in diabetic rats aged 11 months was already thickened in comparison with that in the age-matched male Wistar rats. However in long-term observation, serum creatinine levels did not increased and histologically so-called nodular glomerulosclerosis was not noted.
    This WBN/Kob rat is useful as an animal model of diabetic nephropathy.
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  • Youichi Ikegami, Akito Kitazawa, Haruko Kitaoka, Haruhiko Isotani, Tak ...
    1988 Volume 31 Issue 12 Pages 917-921
    Published: December 30, 1988
    Released on J-STAGE: August 10, 2011
    JOURNAL FREE ACCESS
    The effects of combination therapy with insulin and sulfonylurea on glycemic control were investigated. Fifteen patients with type II diabetes mellitus who did not obtain sufficient glycemic control with sulfonylurea were studied. They were admitted to our hospital and were first treated with insulin alone. Two weeks later, glibenclamide therapy was added to the insulin therapy. Fasting plasma glucose (FPG), FibA1c and urinary glucose levels were measured as paramoters of glycemic control. Daily urinary secretion of c-peptide was also measured as a marker of endogenous insulin secretion. M value was determined from the data on blood glucose of diurnal variance as a parameter of fluctuation of blood glucose levels.
    The mean levels of FPG, HbA1c and urinary glucose were all significantly decreased during 2 weeks of combination therapy. The mean M value was also significantly decreased in this period. The decrease in M value seems to be caused by the improvement of glycemic control in terms of less fluctuation of blood glucose levels, which might be due to an increase in endogenous insulin secretion induced by sulfonylurea.
    The combination therapy may be advantageous in glycemic control for patients with type II diabetes mellitus with sulfonylurea drug failure whose endogenous insulin secretion is reserved.
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  • Mitsuhisa Komatsu, Kunihide Hiramatsu, Toru Aizawa, Takashi Yamada, Ku ...
    1988 Volume 31 Issue 12 Pages 923-928
    Published: December 30, 1988
    Released on J-STAGE: August 10, 2011
    JOURNAL FREE ACCESS
    The therapeutic benefits of sulfonylurea in the treatment of diabetes were evaluated by 1) additional administration of glibenclamide for 48 weeks to patients receiving insulin alone, and 2) withdrawal of glibenclamide from the patients who had been treated with insulin and glibenclamide for 8 weeks. In the first part of the study, the addition of glibenclamide (8.8±0.6 mg/day) had no effect on plasma glucose (PG) and HbA1 in 6 patients (52±6 years old, 2 men and 4 women) without detectable plasma CPR. In 17 patients (61±2 years old, 10 men and 7 women) with measurable plasma CPR, 2-hr postprandial PG and HbA1 were significantly reduced by addition of glibenclamide (9.4±0.3 mg/day)(PG: 310±23 vs 260±16 mg/dl, HbA1: 10.4±0.3 vs 9.6±0.3%). Plasma CPR was significantly increased in this group at 24 weeks (2.4±0.3 to 3.2±0.3 ng/ml) but returned toward the baseline at 48 weeks 2.8±0.5 ng/ml). In the second part of the study, 2 weeks after the withdrawal of glibenclamide (9.1±0.5 mg/day), fasting and postprandial PG were significantly increased (fasting: 131±21 to 223±36 mg/dl, postprandial: 219±11 to 305±41 mg/dl) with decrease in plasma CPR (fasting: 1.8±0.3 to 1.4±0.1 ng/ml, postprandial: 3.8±0.4 to 2.9±0.4 ng/ml).
    Glibenclamide improves glycemic control primarily by enhancing insulin secretion, and insulin/glibenclamide therapy is beneficial for diabetics retaining insulin secretion.
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  • Influence of Renal Failure, Liver Cirrhosis, and Thyroid Dysfunction
    Yasuhiro Sako, Fumio Umeda, Toshihiko Hashimoto, Toyoshi Inoguchi, Kaz ...
    1988 Volume 31 Issue 12 Pages 929-935
    Published: December 30, 1988
    Released on J-STAGE: August 10, 2011
    JOURNAL FREE ACCESS
    Measurement of serum fructosamine (FRA) by means of a Roche kit is a simple and reliable method for estimating glycosylated serum proteins. The level of FRA can be affected by hyperglycemia in diabetics and an abnormal metabolic state of serum proteins such as albumin in patients with renal failure, liver cirrhosis, and thyroid dysfunction. We measured FRA in diabetics and these patients. The average FRA level was 2.58±0.08 (mean±SE) mmol/l in the normal controls (n=18), 4.60±0.67 in patients with IDDM (n=8), and 3.61±0.10 in patients with NIDDM (n=63). In the patients with non-diabetic renal failure, while the FRA level was significantly (p<0.05) low, FRA corrected by total protein concentration was not different from that of the normal controls. The FRA level in liver cirrhosis without hyperbilirubinemia was not significantly different from that of normal controls. In the patients with thyroid disease, the FRA level was 2.08±0.03 in hyperthyroidism and 3.11±0.07 in hypothyroidism. Moreover, the FRA level was negatively correlated with the thyroid hormones T3 and T4 (p<0.001).
    It is concluded that measurement of FRA is clinically useful for evaluating short-term glycemic control in diabetics even when there is complicating nephropathy or liver cirrhosis. However, its level in diabetic patients with hyperbilirubinemia or thyroid dysfunction must be cautiously interpreted.
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  • Kazuhiro Kurasawa, Takao Koike, Yohjiro Itoh, Ryutaro Matsumura, Tatsu ...
    1988 Volume 31 Issue 12 Pages 937-939
    Published: December 30, 1988
    Released on J-STAGE: August 10, 2011
    JOURNAL FREE ACCESS
    We treated young NOD mice (2-week-old) with injections of anti-L3T4 mAb or anti-Lyt-2 mAb in order to elucidate the role of T cell subsets on the development of diabetes in NOD mice.
    Administration of these mAbs prevented insulitis and diabetes in the respective groups of NOD mice. These results were in contrast with our previous report (J. Japan Diab. Soc. 31: 275, 1988) that the administration of anti-L3T4 mAb to precritical NOD mice (12-week-old) prevented diabetes, while anti-Lyt-2 mAb failed to do so, and that severe insulitis similar to that in the control mice was observed in both groups.
    Based on these findings, together with our previous observations, we may conclude that cooperation between L3T4-positive T cells and Lyt-2 positive T cells is essential to the development of insulitis and that L3T4-positive T cells play a major role in the destruction of B cells in NOD mice.
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