Journal of the Japan Diabetes Society
Online ISSN : 1881-588X
Print ISSN : 0021-437X
ISSN-L : 0021-437X
Volume 39, Issue 6
Displaying 1-7 of 7 articles from this issue
  • Naoko Iwasaki, Makiko Kawamura, Hisako Ohgawara, Sachiyo Karibe, Nancy ...
    1996 Volume 39 Issue 6 Pages 409-416
    Published: June 30, 1996
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
    We initiated a genome-wide search for NIDDM susceptibility genes in Japanese by the affected sib-pair approach. This nonparametric method does not require information about the mode of inheritance of the disease gene. Nine candidate genes were tested for linkage with NIDDM in these families: adenosine deaminase (ADA), glucokinase (GCK), insulin (INS), insulin receptor (INSR), β-cell glucose transporter (GLUT2), prohormone converting enzyme2 (PCSK2), β-cell ATP-sensitive K+-channel (KCNJ7), intestinal fatty acid binding protein (FABP2) and muscle glycogen synthase (GSY1). There was no evidence of linkage of any of these genes with NIDDM, implying that they are not major NIDDM-susceptibility loci in Japanese. In addition to investigation of candidate genes, the affected sib pairs are being typed with markers that span the genome. One of the markers tested to date, D2S434, shows some evidence of linkage with NIDDM (p<0.05), suggesting that it will be possible to identify susceptibility loci for NIDDM through genetic studies of affected sib pairs.
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  • A Novel Indicator for Glycemic Control in Diabetes Mellitus
    Kunio Kobayashi, Hirotsune Igimi, Hitoshi Kohno
    1996 Volume 39 Issue 6 Pages 417-424
    Published: June 30, 1996
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
    We propose a novel indicator for diabetic control which reflects the extent of glycation of hair protein (keratin). The glycation index (A390/A412) is based on the ratio of glycated protein-to c ystine-induced coloration, where A390 and A412 represent the absorbance of glycated protein and c ystine in hair protein in color reactions. This index in back and scalp hairs from hypercholestero lemic mice with hyperglycemia, diabetic rats, and diabetic patients yielded significantly higher values (2.0-6.0-fold) than in normal controls (p<0.01). The glycation indices (mean±SD) of the hairs of diabetic andnon-diabetic subjects were 3.00±0.96 (n=22) and 1.51±0.45 (n=34), respectively. These glycation indices (y) correlated well with the levels of glycohemoglobin (HbA1c, x) in the diabetic and non-diabetic subjects: y=0.48x-0.75 (r=0.83, n=34, p<0.01). Within-run precision (reproducibility, CV) for glycation index assay samples of three kinds of hair was 6.7-9. 4%(n=10 each). The proposed hair glycation index provided reasonable rasults for animal and human subjects with normo-and hyperglycemia, suggesting that it is reliable and can be diagnostically useful.
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  • Satoru Tsujii, Mariko Oishi, Yoshiharu Akazawa, Hideshi Kuzuya
    1996 Volume 39 Issue 6 Pages 425-430
    Published: June 30, 1996
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
    A 37-year-old man was admitted to the hospital because of thirst, polyuria, body weight loss and general malaise associated with hyperglycemia (528 mg/dl) and high HbA1c level (12.8%) The neurological findings of drop-foot, steppage gait, muscle weakness and atrophy of the lower extremities, and diminished tendon reflex led to a diagnosis of Charcot-Marie-Tooth (CMT) disease type 1. The diagnosis was confirmed by delayed nerve conduction velocity, and the patient's family history that suggested autosomal dominance. Serum ketone body levels were increased, and serum and urine C-peptide levels were extremely decreased. The serological examination showed positive ICA and GAD antibody. The patient was diagnosed with insulin-dependent diabetes mellitus (IDDM) and was administered insulin, resulting in good glycemic control. The requirement for insulin decreased to 8 units per day but 6 months later was increased to 26 units per day. The association of CMT disease and IDDM in one patient is very rare, and there has been no reports that involve anti-GAD positive IDDM. A potential association between CMT disease and IDDM via a common mechanism is not yet known, but may become clearer following the recent characterisation of the molecular basis of CMT disease type 1.
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  • Masahiko Sawada, Taro Maruyama, Yoshiaki Kitazawa, Norio Maeda, Ryoji ...
    1996 Volume 39 Issue 6 Pages 431-437
    Published: June 30, 1996
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
    The patient was an 18-year-old obese male who had been consuming soft drinks in excess of 3L/day since the spring of 1993. In early October, he experienced difficulty breathing and was admitted to our hospital in a delirious state on October 14. His body mass index was 44.8 kg/m2, plasma glucose level was 1040 mg/dl, and severe metabolic acidosis was present. Neither IDDM-associated HLA types, islet-cell antibodies (ICA) or anti-GAD 65 antibodies were found. We made a diagnosis of diabetic ketoacidosis and immediately started intravenous insulin infusion and fluid replacement. Although the hyperglycemia improved, the metabolic acidosis did not, the dyspnea worsened, and oxygenation deteriorated rapidly. The patient died 10 hours after admission. At autopsy, the main pulmonary arteries were found to be obstructed by thrombi. In the pancreas, islets were decreased in number, but there was no insulitis. Severe loss of β-cells was prominent with aldehyde fuchsin staining. Mild diabetic nephropathy was also identified. These pathological findings suggest that glucose toxicity may produce morphological damage in pancreatic β-cells.
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  • Yoshikazu Umeno, Kazuhiko Kogawa, Mikiyo Johjima, Yoshiro Ohta
    1996 Volume 39 Issue 6 Pages 439-444
    Published: June 30, 1996
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
    A 72-year-old man who was being treated for diabetes mellitus (DM) developed myasthenia gravis (MG) at the age of 38. Treatment with neostigmine improved the MG, but his DM had been poorly controlled. In November 1994, the patient was readmitted to our hospital with chief complaints of blepharoptosis, and weakness of neck and lower extremities, a diagnosis of MG, generalized form, was made. Oral administration of ambenonium chloride and prednisolone was effective. In April 1995, the patient felt a tumor in his left abdomen. Ultrasonography and computed tomography showed an abscess in the left abdominal wall. The abscess was aspirated, and a specimen from it yielded Nocardia farcinica on culture. Pulmonary infection and brain abscess were found in addition to the abscess, and the patient developed pulmonary tuberculosis. The infections were treated by surgical drainage and antibiotics, and the patient was able to control his glucose levels with insulin. Nocardiosis has been reported to be an uncommon disease in DM patients, however, it should be considered when DM patients are treated with corticosteroids.
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  • 1996 Volume 39 Issue 6 Pages 445-484
    Published: June 30, 1996
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
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  • The Third Report of the GHb Standardization Committee, the Japan Diabetes Society
    Kenji Shima, Jiro Endo, Munetada Oimomi, Yasue Omori, Yoshiaki Katayam ...
    1996 Volume 39 Issue 6 Pages 485-493
    Published: June 30, 1996
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
    The Glycohemoglobin (GHb) Standardization Comittee conducted the third external quality assessment to evaluate the interlaboratory variation of GHb values measured by various methods including HPLC, turbidimetric inhibition immunoassay (TINIA) and affinity chromatographic methods in 1, 424 institutes throughout the country using four samples (2 concentrated whole blood and 2 lyophilized hemolysate). In addition, we compared our assay values to Diabetes Control and Complications Trial (DCCT) values by measuring the same 48 fresh blood samples in the laboratory of Tokushima Univ. and in theirs.
    We got the following results, 1) The CVs as indices of the interlaboratory variation ranged from 7.1% to 12.8% when all data were combined. It was different depending on an analytical method used: HPLC, 3.7-6.5%; T INIA, 7.6%-11.7%; Affinity 5.6%-6.4%.
    2) The means of the measured values were different depending on a method used. The value measured by HPLC (4.7±0.31%) was similar to that by TINIA (4.9±0.56%), but the value measured by an affinity chromatographic method (5.5±0.31%) was signficantly higher than the others.
    3) The CVs among the GHb value corrected with the assigned values of Japan Diabetes Society (JDS) calibrators ranging from 4.6% to 7.8%, were much smaller than those corrected with other calibrators or without correction, 8.3% to 15.9%.
    4) Our measured values were quite similar to DCCTs': The values measured by Tosoh=0.984 X DCCT-0.228; r=0.998, Ones by Kyoto Daiichi =0.972×DCCT-0.052, r=0.997) In conclusion, the correction of measured GHb values with the assigned values of the calibrators provided by JDS is useful to reduce the interlaboratory variation to a clinically permissible level and to get a good agreement between our values and DCCT's.
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