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Volume 41, Issue 6
Displaying 1-8 of 8 articles from this issue
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Toshiro Shibata, Eiji Suzuki, Kikuko Yasuda, Keigo Yasuda1998 Volume 41 Issue 6 Pages 423-431
Published: June 30, 1998
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSThe purpose of this study was to investigate the effects of aldose reductase inhibitor (ARI) on metabolic derangement and prostaglandin I2 analogue (PGI2) on vascular lesions in diabetic neuropathy by using magnetic resonance imaging (MRI)(SIGNA 1.5-Tesla). Spin-lattice relaxa tion time (Ti value) and coefficients of variation of signal intensities of nerve (CV value), as respective indices of nerve edema and structural change in the sural nerve, were calculated in normal subjects (n=19) and patients with non-insulin-dependent diabetes mellitus (DM group)(n=92). The T1 value of the sural nerve was significantly prolonged in the DM group indicating the presence of nerve edema under hyperglycemic conditions. Administration of ARI (Epalrestat 150mg/day, n=12) improved the nerve edema as well as motor nerve conduction velocity (MNCV). There was no difference in Ti values before and after PGI2 treatment (Beraprost sodium 120μg/day, n=12), but MNCV significantly improved. In patients with longer T1 values, PGI2 normalized them. These results suggest that both metabolic and vascular factors participate in the pathogenesis of nerve edema. The CV value was significantly increased in the DM group. The CV value also increased in proportion to the progression of diabetic retinopathy and nephropathy, suggesting that increased CV values may reflect changes in endoneurial structure caused by microangiopathy. These results indicated that ARI and PGI2 can ameliorate diabetic neuropathy by improving metabolic and vascular abnormalities, and that T1 and CV values plus MRI are useful indicators for evaluation of structural changes in diabetic neuropathy and the efficacy of treatment.View full abstractDownload PDF (1255K) -
An Application of HOMA's IndexHiroyuki Hosojima, Kenzo Uchida1998 Volume 41 Issue 6 Pages 433-441
Published: June 30, 1998
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSAlthough several methods of evaluation have been developed to quantify insulin sensitivity and resistance in patients with impaired glucose tolerance (IGT) or diabetes, they are complicated expensive, and patient poorly tolerated by patients, and as a result not used in outpatient clinics. In order to find a simple index for evaluating insulin resistance in IGT and diabetes, we investigated the usefulness of an index of insulin resistance obtained by applying a Basal Homeostasis Model Assessment (HOMA) equation in 40 obese subjects with IGT (OIGT), 46 non-obese subjects with IGT (NIGT), and 18 control subjects with normal glucose tolerance (C). Obesity was defined as a BMI of 26.4kg/m2in men and 25.8kg/m2in women. HOMA insulin resistance index (HOMA-R) was obtained by solving the equation: FIRI/22.5 e-InFpG.
The BMI and glycohemoglobin (HbAic) was 28.4±0.4 kg/m2 and 5.5±0.1%, respectively, in OIGT, 22.4±0.3kg/m2 and 5.6±0.1% in NIGT, and 21.9±0.2kg/m2 and 5.3±0.1% in C. Hyperinsulinemia, hyperlipidemia, and high blood pressure were present in OIGT, but no differences in HbAic or fasting blood glucose were found between the groups. On the other hand, HOMA-R was 3.1±0.2 (mU·mmol/12) in OIGT, 2.0±0.1 in NIGT, and 1.4±0.1 in the control, and significantly higher in OIGT than in the other groups. HOMA-R in NIGT was also significantly higher than in the control. HOMA-R was positively correlated with BMI, FIRI, FPG, I PG, I IRI, I IRI/I PG, MaxPG, Ma×IRI, and Ma×IRI/Ma×PG, and the correlation coefficient between HOMA-R and FIRI was strongly positive (γ=0.913)
Thus, HOMA-R appears to be a useful and simple index of insulin resistance in obese and nonobese IGT and NIDDM subjects. It is a near approximation of the glucose infusion rate in the euglycemic glucose clamp method. HOMA-R clearly has some limitations and disadvantages when used; 1) in IDDM subjects, 2) in NIDDM subjects with suppressed insulin secretion, or 3) in diabetic subjects with insulin abnormality or insulin receptor abnormality.View full abstractDownload PDF (1113K) -
Reiko Kawahara, Masayo Yoshino, Yoshimasa Tasaka, Noriko Nagase, Chizu ...1998 Volume 41 Issue 6 Pages 443-447
Published: June 30, 1998
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSThe relationship between plasma leptin levels and insulin resistance was studied in 66 obese subjects (23 men, 43 women) aged 42.3±13.8 yrs (mean±SD) with a body mass inde×(BMI) of 33.0 ×5.4kg/m2.
The subj ects were divided into the following three groups according to WHO criteria for 75-g OGTT: normal glucose tolerance (NGT, n=27); impaired glucose tolerance (IGT, n=16); and diabetic (DM, n=23). Plasma leptin levels were measured with a human leptin RIA kit, insulin resistance (IR) and fl-cell function (β-CF) were calculated by using the HOMA model of Matthews et al. The results were as follows 1. Plasma leptin concentrations in obese subjects were higher in women than in men. 2. The plasma leptin levels in the three obese groups were similar, with no significant differences. 3. There were significant correlations between plasma leptin concentrations and BMI, % body fat, fasting insulin levels and insulin resistance. 4. The plasma leptin level is significantly related to insulin resistance, independently of adiposity. Therefore we conclude that elevated plasma leptin concentrations in the presence of obesity might contribute to insulin resistance but do not influence glucose metabolism.View full abstractDownload PDF (737K) -
Sayaka Honda, Takako Saito, Akio Kawakami, Tomoatsu Nakamura, Kumiko R ...1998 Volume 41 Issue 6 Pages 449-454
Published: June 30, 1998
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSA 55-year-old man with non-insulin dependent diabetes mellitus was admitted to Jichi Medical School Hospital in order to control his hyperglycemia. He had taken 500mg of chlorpropamide daily for 7 years. His laboratory data showed serum Na, 131 mEq/l;urinary excretion of Na, 88mEq/day;and urinary osmolality, 479 mOsm/kgH2O. An acute water loading test detected impaired water excretion. After chlorpropamide was ceased, the serum Na level normalized in assoc-iation with improvement of renal water excretion. There was no elevation of the plasma arginine vasopressin (AVP) level. These results suggest that chlorpropamide augments the renal action of AVP, providing a pathological condition-like syndrome of inappropriate secretion of antidiuretic hormone.View full abstractDownload PDF (672K) -
[in Japanese], [in Japanese], [in Japanese], [in Japanese], [in Japane ...1998 Volume 41 Issue 6 Pages 455-459
Published: June 30, 1998
Released on J-STAGE: March 02, 2011
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[in Japanese], [in Japanese], [in Japanese], [in Japanese], [in Japane ...1998 Volume 41 Issue 6 Pages 461-466
Published: June 30, 1998
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESS -
Kazuo Sonoki, Kimie Nishiyama, Yuichi Satou, Hiroshi Tsuruta, Kaoru On ...1998 Volume 41 Issue 6 Pages 467-474
Published: June 30, 1998
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSA 26-year-old man was diagnosed with NIDDM in 1991. Since his mother had diabetes and deaf as well, we tested him for mitochondrial DNA and detected the 3243bp mutation. In 1994, he developed the nephrotic syndrome (BUN 16.4 mg/d/, Cr 0.8 mg/dl, Ccr 39.6 ml/min.) without retinopathy, and a renal biopsy was performed. Light microscopy showed mild mesangial expansion that seemed to represent diabetic nephropathy, but in addition to segmental sclerosis, immunofluorescent staining showed granular deposition of IgM and Ciq, and Electron microscopy revealed dense deposits. Asa result, the renal lesion was concluded to be accompanied by focal segmental sclerosis. On March in 1996, the patient was admitted with dyspnea, cough, and edema. His renal function had rapidly deteriorated to end-stage. We examined the renal biopsy specimen again, and found that the kidney was in the histological endstage. Hemodialysis was instituted in July, five years after thediagnosis of diabetes. The rapid deterioration in renal functionseemed to be attributable to the mitochondrial gene mutation in addition to the poor glycemic control (HbAic 8.3%-16.7%) and insufficient restriction of protein intake.View full abstractDownload PDF (6598K) -
[in Japanese]1998 Volume 41 Issue 6 Pages 475-490
Published: June 30, 1998
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSDownload PDF (3650K)
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