Journal of the Japan Diabetes Society
Online ISSN : 1881-588X
Print ISSN : 0021-437X
ISSN-L : 0021-437X
Volume 39, Issue 2
Displaying 1-11 of 11 articles from this issue
  • Akihisa Iguchi
    1996 Volume 39 Issue 2 Pages 85-90
    Published: February 29, 1996
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
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  • Mikihiko Kudo, Ken-ichi Kimura, Naoko Yamada, Masayuki Ishigame
    1996 Volume 39 Issue 2 Pages 91-96
    Published: February 29, 1996
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
    We studied 190 diabetics to examine a prevalence of the peripheral arterial occlusive disease of low extremities. The ankle blood pressures at the dorsalis pedis artery and the tibialis posterior artery were measured using Doppler ultrasound. The ankle-brachial pressure index (API) which is a ratio of the ankle systolic pressure/the brachial systolic pressure, was calculated. Arteriographic studies were performed in the patients who showed the index of less than 0.90. Peripheral arterial occlusive disease was diagnosed by API of less than 0.90 and significant stenosis (<50% of diameter) or occlusion in the arteriogram.
    The prevalence of peripheral arterial occlusive disease was 8.4 percent (16 of 190 patients). More specifically the prevalence rates were 3 percent (2 of 78) of the normoalbuminuria group (albumin-creatinine ratios of less than 29mg/g), 7 percent (5 of 71) of the micro-albuminuria group (the ratios of 30 to 299mg/g) and 20 percent (9 of 41) of the macroalbuminuria group (the ratios of 300 mg/g or greater).
    Based on correlation analysis, API was increasingly positively related to HbA1, hyperlipidemia (intake of lipid-lowering drugs), ex-smoking (no smoking at present, but smoking in the past), systolic blood pressure, and smoking at present.
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  • Naoki Sakane, Toshihide Yoshida, Tunekazu Umekawa, Motoharu Kondo
    1996 Volume 39 Issue 2 Pages 97-103
    Published: February 29, 1996
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
    One hundred and seventeen obese diabetic female patients were subjected to the measurement of scores in stress check list and daily hassles scale, indicators of stress state and stressors. Forty-one patients were assessed as stressful by these tests, and these were divided into two groups; one group was educated only on diet and exercise therapies, and the other group received combined stress management therapy including diet and exercise. Seventy-six non-stressful patients were also given diet and exercise therapies. One year after these treatments, the obese diabetic (non-stress) and obese diabetic (stress+stress management) groups significantly reduced body weight, body mass index, HbA1c, plasma glucose area, and insulin area during OGTT. However, the obese diabetic (stress) group did not reduce body weight and their scores on the stress check list deteriorated.
    These findings indicate that this combined stress management therapy is effective in 1) correction of stress state, 2) maintaining weight loss and 3) improving diabetes mellitus in obese diabetic patients with mental stress. These results suggest that this therapy would be useful in the treatment of obese diabetic women who cannot reduce their body weight because of stress and stress-induced hyperphagia.
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  • Kazunari Matsumoto, Yoshihiko Yamaguchi, Shoichi Akazawa, Norio Abiru, ...
    1996 Volume 39 Issue 2 Pages 105-111
    Published: February 29, 1996
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
    We investigated the C-peptide response (CPR) to a 400 kcal mixed meal (carbohydrate 60%, protein 20%, lipid 20%) before and after treatment in non-insulin-dependent diabetes mellitus (NIDDM) subjects. Forty NIDDM subjects were classified into three groups according to their pretreatment fasting plasma glucose (FPG) levels: Group A (n=11), FPG<140mg/dl; Group B (n=19), 140≤FPG<200mg/dl; and Group C (n=10), 200mg/dl≤FPG. After the treatment periods of 4-8 weeks, the plasma giucose curve during the mixed meal loading test significantly improved in all groups. The CPR response during the mixed meal test significantly increased in Groups B and C after treatment, but was not changed in Group A. The subjects with FPG levels above 140mg/dl (Group B and C). were classified into three groups according to the methods of treatment. The three groups were as follows: Treated diet alone (n=8), an oral hypoglycemic agents (OHA)(n=6), and an insulin treatment (n=15). The CPR response at 120min after mixed meal load (CPR 120) significantly increased after treatment in the subjects given a treated diet alone (4.8±1.6 to 6.1±0.8ng/ml, p<0.01). Similarly, in both the subjects treated with OHA and insulin, the CPR 120 significantly increased (3.9±0.4 to 5.1±0.5 and 2.8±0.3 to 4.1±0.3ng/ml, p<0.05 and p<0.01, respectively). In summary, impaired insulin secretion recovered by the good glycemic control in NIDDM with fasting hyperglycemia, and improvenment in insulin secretion was independent of the methods of treatment.
    Therefore, when post-prandial CPR level is applied for the evaluation of insulin secretion, the levels of hyperglycemia in NIDDM subjects should be considered.
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  • Hidenobu Sakaguchi, Tokio Sanke, Sinya Ohagi, Kishio Nanjo
    1996 Volume 39 Issue 2 Pages 113-121
    Published: February 29, 1996
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
    Recently, several case reports have suggested that mutations in mitochondrial DNA, especially substitution of A to G at position 3243 of leucine tRNA (3243 mutation), may cause diabetes and deafness. We discussed the feasability of mass screening to detect the 3243 mutation using genomic plasmid DNA by the competitive PCR method. We found that the proportion of mutated DNA was as much as 1% artificial heteroplasmy by using the nonradioactive PCR/ RFLP method, but templates having minimal mutant plasmid were estimated more crudely than the amount of the known mutant concentration rate. We next applied the allele specific oligonucleotides reported previously to the detection of this mutaion, but were unsuccessful. We have no clear explanation for the lack of success.
    We studied 300 patients with the common form of non-insulin-dependent diabetes mellitus (NIDDM), two patients with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) and 250 non-diabetic controls. We identified the 3243 mutation in two patients with MELAS, but no such mutation was detected in either 300 NIDDM patients or 250 controls. The two patients had poor insulin secretory responses to glucose.
    These results suggest that the frequency of the mitochondrial 3243 mutation may be very low in the common form of NIDDM.
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  • Ryohei Todo, Naomi Todo, Tomoko Shinoda, Masako Morita, Shigenobu Ishi ...
    1996 Volume 39 Issue 2 Pages 123-128
    Published: February 29, 1996
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
    Using a Cochet & Bonnet aesthesiometer, we investigated the usefulness ofcorneal sensitivity as a quantitative index of sensory neuropathy in diabetic patients.
    In 68 normal volunteers, corneal sensitivities were 50mm or more in their 60's oryounger, while being significantly decreased in their 70 and 80's. In 167 NIDDM patients, corneal sensitivities were significantly decreased in their 40's, 50's and 60's as compared with those in the same age groups of normal volunteers.
    The relationships between corneal sensitivity and other indices of diabetic complications, such as subjective symptoms of sensory neuropathy, the coefficient of variation of R-Rintervals on electrocardiograms, microalbuminuria, retinal status, duration of diabetes and treatments for diabetes were statistically significant. When comparisons were made between age-and sex-matched groups with normal corneal sensitivity and those with decreasedcornealsensitivity, motorand sensory nerve conduction velocities were found to be significantly decreased in the latter. Multiple regression analysis indicated that diabetic retinopathy and subjective symptoms of sensory neuropathy were significantly related to corneal sensitivity.
    These data suggest that measurement of corneal sensitivity offers a simple and quantitative test of sensory neuropathy in diabetic patients.
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  • Masateru Nishiki, Satoshi Ohguni, Keiichiro Tanigawa, Katsuhiro Tamura ...
    1996 Volume 39 Issue 2 Pages 129-135
    Published: February 29, 1996
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
    A 66-year-old woman was admitted to our department for general fatigue and weight loss. She had received total pancreatectomy at age 64yr and was treated with intensive insulin therapy in combination with intramuscular injection of glucagon (1mg) at 2300h. However, plasma glucose (PG) was not well controlled and plasma gluconeogenic precursors (lactate, pyruvate and amino acids), non-esterified fatty acids (NEFA) and total ketone bodies were remarkably elevated. Strict control of PG for 24hrs using an artificial pancreas (AP) normalized plasma levels of NEFA and total ketone bodies, but had no effect on plasma lactate, pyruvate and glucogenic amino acids. Subcutaneous injection of 0.1mg glucagon at 2300h while under strict PG control by AP normalized plasma lactate and pyruvate but not plasma NEFA and total ketone bodies. Continuous subcutaneous infusion (CSI) of glucagon 0.1mg for 8hrs starting at 2300h while under strict PG control by AP normalized plasma NEFA, total ketone bodies and most glucogenic amino acids.
    These findings suggest that strict control of PG in combination with CSI of a small dose of glucagon is effective for correcting abnormal metabolism in diabetic patients after total pancreatectomy.
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  • K Aoki, T Babazono, A Saeki, T Wasada, S Teraoka, K Ota, Y Omori
    1996 Volume 39 Issue 2 Pages 137-145
    Published: February 29, 1996
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
    To clarify the effect of pancreas transplantation on insulin sensitivity in patients with insulin-dependent diabetes mellitus (IDDM), glucose infusion rates (GIR) were determined using the euglycemic hyperinsulinemic clamp technique in 6 kidney and pancreas transplant (PKT) recipients, 19 normal subjects, 14 IDDM patients without nephropathy, 16 IDDM patients receiving dialysis, and 6 IDDM patients after solitary kidney transplantation. Five of the 6 PKT recipients were studied before and serially after pancreas transplantation. In the 5 PKT patients, GIR increased significantly from the pretransplant value of 3.68±1.47mg/kg/min to 5.54±1.11mg/kg/min two months after transplantation despite immunosuppressive treatment and hyperinsulinemia. The GIR remained within the mean±1SD of the GIR for normal sublects so long as the pancreatic grafts were fully functional. Although GIRs in the three control IDDM groups were significantly lower than that in normal subjects (6.95±1.57mg/kg/min), GIR in the 6 PKT recipients (6.43±1.00mg/kg/min) did not differ from that in normal subjects. We conclude that pancreas transplantation improves glucose metabolism in patients with long-standing IDDM not only by restoring insulin secretion but also by reducing peripheral insulin resistance.
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  • Hiroyuki Shimizu, Mayumi Negishi, Ken-Iich Ohtani, Yoshito Tanaka, Nor ...
    1996 Volume 39 Issue 2 Pages 147-151
    Published: February 29, 1996
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
    Hypercoagulability may increase the risk of cardiovascular disease (CVD) in diabetic patients with albuminuria. Plasma Thrombin-Antithrombin III complex (TAT) levels, representing the functional state of the clotting system, were studied in 127 non-insulin-dependent diabetic (NIDDM) patients. The patients were divided into three groups according to the urinany albumin index (UAI: mg/g Cr): Group A; UAI≤20, Group B; 20<UAI≤200, Group C; UAI>200. The frequency of patients with increased TAT levels increased with the increment of UAI. The average UAI in gnoup C was significantly increased as compared to that in gnoup A. Plasma TAT levels correlated significantly with UAI and HbA1c levels. These data indicate that the degree of diabetic albuminuria correlates with plasma TAT levels in NIDDM patients and that the observed hypercoagulability may be involved in the increased frequency of CVD in NIDDM patients with albuminuria.
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  • Tsutomu Kanda, Eiichi Imano, Hiroyuki Matsushima, Masahiko Wada, Rieko ...
    1996 Volume 39 Issue 2 Pages 153-159
    Published: February 29, 1996
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
    We encountered an NIDDM patients with the complication of postprandial hypotension (PPH) who repeatedly experienced syncope after meals. The patient was successfully treated with amezenium methylsulfate which increased endogenous norepinephrine levels and blood pressure.
    The patient, a 66-year-old woman, was diagnosed with NIDDM in 1971 and treated with oral hypoglycemic agents. Thereafter, she maintained poor glycemic control. Since she repeatedly experienced post prandial syncope with palpitation which lasted up to ten minutes and occurred once or twice amonth beginning in February 1993, she was hospitalized in August 1993. We noted that she had a history of syncope after meals, and performed 24-hour ambulatory blood pressure monitoring (AMBP) and 2-hour AMBP during a 75g oral glucose tolerance test (OGTT). She was diagnosed with NIDDM complicated by PPH based on complaints of general fatigue as well as a systemic blood pressure (SBP) decrease of 25mmHg. The concentrations of plasma norepinephrine (NE) were 338pg/ml before OGTT and 268pg/ml after OGTT. When she was given 10mg of amezinium methylsulfate (AM) per os 2hours before OGTT, the decrease in SBP was only 12 mmHg. The patient had no further complaints and plasma NE concentrations increased from 290 pg/ml before OGTT to 348pg/ml after OGTT.
    These results indicate that PPH in this case was caused by the intake of meals including glucose. PPH improved rapidly with AM administration which increased plasma NE.
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  • [in Japanese], [in Japanese], [in Japanese], [in Japanese], Ronald E P ...
    1996 Volume 39 Issue 2 Pages 160-161
    Published: February 29, 1996
    Released on J-STAGE: March 02, 2011
    JOURNAL FREE ACCESS
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