Journal of the Japan Diabetes Society
Online ISSN : 1881-588X
Print ISSN : 0021-437X
ISSN-L : 0021-437X
Volume 43, Issue 6
Displaying 1-11 of 11 articles from this issue
  • Toshihisa Morimoto, Junko Sawa, Muneyoshi Yoshida, Toshiki Hozumi, Ken ...
    2000 Volume 43 Issue 6 Pages 421-430
    Published: June 30, 2000
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
    Wheat albumin (WA), which has anti-a-amylase activity, delays carbohydrate digestion and reduces postprandial glycemic increases. The effects of long-term WA administration on carbohydrate metabolism and histology were investigated in 50mg/kg BW-Streptozotocin-induced diabetic rats. In Study 1, diabetic rats were fed a high starch (HS) diet (P: F: C=20: 10: 70) with or without 5% WA for 10 weeks. The feed supply was controlled so that both groups received the same energy intake. WA administration was found to accelerate gains in body weight (p=0.02, ANOVA) and lower the 2-hour blood glucose level in an OGTT after 9 weeks (p=0.006). In Study2, healthy and diabetic rats were fed a diet with an energy similar to that of Japanese standard (JS, P: F: C=16: 25: 59) with or without 5% WA ad libitum for 10 weeks. Diabetic rats showed slower gains in body weight (p<0.001) despite a larger energy intake (p<0.001) compared to healthy rats. The reduced body weight gain seen in diabetic rats was significantly increased by WA administration (p<0.001). Furthermore, the increasse in fructosamin seen in diabetic rats was suppressed by WA (p=0.02). In both sudies, the number of remaining beta-cells in the pancreatic tissue of diabetic rats who received WA was higher than in diabetic control rats. These results indicate that the longterm administration of WA could be beneficial in controlling the metabolism of carbohydrates in diabetics.
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  • Kayoko Nomura, Hisaya Tada, Koji Kuboki, Toshiki Inokuchi
    2000 Volume 43 Issue 6 Pages 431-436
    Published: June 30, 2000
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
    We investigated the effect of TGF-β1 latency-associated peptide (LAP) on the glucose-induced increase in extracellular matrix proteins in cultured human mesangial cells (MC). Recombinant LAP suppressed TGF-β1 lactivity in the absence of MC in a dose-and time-dependent manner. LAP treatment prevented the TGF-Β1-induced increase in the fibronectin (FN) production of MC. The exposure of MC to 33mM of glucose resulted in an increase in FN and thrombospondin (TSP) production compared to the levels resulting from exposure to5mM of glucose. The glucose-induced overproduction of FN and TSP was completely suppressed by concomitant treatment with LAP. The addition of LAP to MC cultured with a low-glucose media showed no demonstrable effects on the production of FN and TSP.
    These results indicate that the glucose-induced increase in FN and TSP production in MC is prevented by LAP through the suppression of TGF-β1 activity. These findings warrant further in vivo study on the effects of LAP in diabetic nephropathy.
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  • [in Japanese], [in Japanese], [in Japanese], [in Japanese], [in Japane ...
    2000 Volume 43 Issue 6 Pages 437-441
    Published: June 30, 2000
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
  • Hiroyuki Ariyasu, Norihiko Murakami, Nobuyuki Azuma, Sumiko Kato
    2000 Volume 43 Issue 6 Pages 443-448
    Published: June 30, 2000
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
    A 20-year-old woman with Type-1diabetes mellitus was admitted to Kishiwada City Hospital due to pancreatitis. On the 56th hospital day, she had left-sided hemiparesis accompanied by hypoglycemia, and normalization of blood glucose level by glucose administration resulted in disappearance of the hemiparesis. On the 63rd hospital day, right-sided hemiparesis occurred with hypoglycemia, and the paresis also disappeared after glucose administration. Head CT, head MRI and magnetic resonance angiography showed no abnormal findings. Taken together with the clinical course, it was concluded from these results that the repeated hemiparesis was due to hypoglycemia. This case seems to be rare. However, we should be aware that hypoglycemia may be a cause of hemiparesis in patients with insulin-treated diabetes mellitus. In addition, the mechanism remains controversial and further examinations are required
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  • Keiko Ashidate, Mitsunobu Kawamura, Masatoshi Ishii, Kazumasa Hase, Hi ...
    2000 Volume 43 Issue 6 Pages 449-454
    Published: June 30, 2000
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
    A 38-year-old man was diagnosed as having type-2 diabetes at the age of 30 years, and his glycemic control was consistently poor. The patient was referred to our hospital in September1994because of oral white plaques, dysgeusia, and dysphagia. Esophago-gastroendoscopy was performed, and a diagnosis of oral and esophageal candidiasis was made. Antifungal drugs were administered, but they were not very effective. The patient was admitted to our hospital for glycemic control and treatment of candidiasis in March 1998. Multiple daily injections of insulin were performed, improvement in glycemic control was achieved, and the candidiasis resolved. After discharge, his glycemic control worsened, and he experienced a recurrence of oral candidiasis. Esophageal candidiasis has been reported in immuno-compromised hosts, and diabetic patients with poor control and/or severe autonomic neuropathy are said to be extremely susceptible to it. Although our patient was not immunodeficient, he did have recurrent candidiasis. Antifungal drugs were not very effective, but improvement in the hyperglycemia rapidly cured the candidiasis. This suggests that intensive glycemic control is important for the prevention and treatment of infection in diabetic patients.
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  • Michiko Togashi, Hitomi Yamada, Naoko Iwasaki, Hiroki Yokoyama, Asako ...
    2000 Volume 43 Issue 6 Pages 455-458
    Published: June 30, 2000
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
    We report an autopsy case of a 47-year-old diabetic woman with MELAS. After the onset of deafness at the age of 25 years, diabetes, dilated cardiomyopathy, renal failure, dysarthria, syncope, and muscle weakness gradually progressed. The diabetes and deafness were maternally inherited. The patient was admitted because of syncope and shoulder pain. Her renal failure was so severe as a result of rhabdomyolysis that hemodialysis was instituted. However, the patient died of sepsis on the6th hospital day. Pathological examination showed characteristic findings of MELAS, such as ischemic change and calcification of the basal ganglia in the brain, ragged-red fibers in the skeletal muscles, and smooth muscle degeneration. The proportion of mitochondria with the 3243 mutation was 38% in the pancreas, 14% in the peripheral blood, and more than 50% in the brain, heart, liver, stomach, and kidney. Hematoxylin-eosin staining of the pancreas showed that the islets were atrophic, and their acidophilicity made it difficult to discriminate the islet contours from the exocrine tissue. Immunohistochemical staining showed a marked decrease in the number of β-cells, but α-cells were well maintained. These findings contrast with previous reports that both α and β cells were equally atrophic in cases with MELAS.
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  • Michiko Hayakawa, Kazuyoshi Kajimoto, Toshiki Hozumi, Wataru Sano, Aki ...
    2000 Volume 43 Issue 6 Pages 461-466
    Published: June 30, 2000
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
    We report a 30-year-old woman with slowly progressive Type-1 diabetes complicated by an eating disorder after strict dietary intervention. Diabetes was frst diagnosed at the age of 26 years, and excellent glycemic control was achieved by stric tdietary intervention during the subsequent 2 years, although the patient's weight decreased from 50 to 36kg (BMI: from 21.1 to 15.2kg/m2) and she developed amenorrhea.
    At the age of 30 years she was admitted because of ketoacidosis after 2 years off medication. Her serun contained high levels of antibody to GAD, and daily urinary CPR excretion was extremely low (0.59μg day), showing that she had slowly progressive Type1 diabetes. Although the ketoacidosis was successfully treated and excellent glycemic control was achieved with insulin, the patient developed severe anorexia without bulimia, and her weight decreased to 31kg (BMI: 13.0kg/m2). Intravenous hyperalimentation was necessary to maintain and increase her weight. Psychological examination revealed no abnormalities. We believe that her eating disorder may have been related to the strict dietary intervention.
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  • Shimpei Fujimoto, Hideaki Tsukada, Masaya Hosokawa, Mariko Kajikawa, J ...
    2000 Volume 43 Issue 6 Pages 467-471
    Published: June 30, 2000
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
    A 70-year-old woman who had been treated with insulin for 24 years was admitted for control of diabetes mellitus. Because no intrinsic insulin secretion was detected and the anti-GAD antibody level was high (259U/ml), the patient was treated as a type-1 diabetic. Two weeks after admission, glycemic control worsened and the patient complained of hidrosis. A diagnosis of Graves' disease was made based on a high free T4 level, low TSH level, and positivity for TSH-binding inhibitor immunoglobulins in the patient's serum. She was treated with thiamazole and became euthyroid, and the insulin requirement decreased as her thyroid function improved. Diffuse atrophic gastritis of the body of the stomach was observed on an endoscopic examanation, and positivity for anti-intrinsic factor antibody in her serum suggested autoimmune gastritis. Although the serum vitamin B12 level was mormal and no evidence of pernicious anemia was found, the patient will be monitored for it in her follow-up examinations.
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  • [in Japanese], [in Japanese], [in Japanese], [in Japanese], [in Japane ...
    2000 Volume 43 Issue 6 Pages 473-476
    Published: June 30, 2000
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
  • Kyuzi Kamoi, Nobuya Fujita, Yoshihiro Ikezawa, Masato Takagi, Hideo Sa ...
    2000 Volume 43 Issue 6 Pages 477-481
    Published: June 30, 2000
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
    We describe a case of type-1diabetes with the mitochondrial DNA 3243 (A to G) mutation in which the restriction of daily physical activity improved glycemic control. Our patient is a 56-year-old woman with a point mutation (3243 A to G) in the mitochondria of her leukocytes. The patient has a short stature and slender figure and does not exhibit clinical myopathy or any central nervous system disordes. Two of her sons have the same mutation but do not exhibit either diabetes mellitus or hearing loss.
    At the age of 38, our patient began to experience sensory hearing loss. Two years later, insulin therapy was initiated. At the age of 52, she developed chronic thyroiditis. An anti-GAD antibody test was positive, and her HLA was A 24, DR 4 and DQA1*0301. Although the HbAic level had been maintained at 8-9.4% for 15 years, few chronic complications of diabetes had been observed. The serum concentrations of lactate and pyruvate were elevated and increased markedly during and after exercise on a bicycle ergometer, suggesting the presence of myopathy at a subclinical level. The HbA1c level decreased gradually after the patient began to restric her daily physical activity level, and no change in her required insulin dose was necessary. After one year of restricted daily physical activity, the patient's HbAic level was 6.5%. The restriction in daily activity also attenuated the response of the lactate and pyruvate serum levels during periods of exercise on a bicycle ergometer. The restriction of physical activity would suppress ATP utilization and may improve glucose control in this case, since the production of ATP is disturbed by the mitochondrial DNA 3243 mutation.
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  • 2000 Volume 43 Issue 6 Pages 483-525
    Published: June 30, 2000
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
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