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Volume 30, Issue 2
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[in Japanese]1987 Volume 30 Issue 2 Pages 103
Published: February 28, 1987
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSDownload PDF (128K) -
Relation to Beat-to-beat Variation in Heart Rate (CVR-R) at RestTakashi Ohoshi1987 Volume 30 Issue 2 Pages 105-112
Published: February 28, 1987
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSExercise tolerance tests were given to patients with non-insulin-dependent diabetes mellitus (NIDDM) to evaluate their metabolic, hormonal and sympathetic responses to exercise.
The 27 subjects had neihter proliferative retinopathy nor renal dysfunction. Most of them were engaged in light work and had not participated in physical training programs.
After fasting for about 14 hours, the subjects were loaded with bicycle ergometer exercise (1 watt/kg ideal body weight) for 20 min. Blood and urine samples were collected at 30 min after supine rest (“0 min”), at cessation of exercise (“20 min”) and at 30 min aftr ccsstion (“50 min”). Glucose, FFA, 3-hydroxybutyrate (3-OHBA), lactate, IRI, IRG, HGH, and cortisol in blood were determined. Noradrenaline (NA) and adrenaline (Adr) in urine were determined by the HPLC-THI method. The excretion rate of each catecholamine in each period was divided by the creatinine clearance value in the corresponding period.
Multiple regression analysis showed that the responses of FM from 0 to 50 min (Δ50), 3-01-IBA (Δ50), cortisol from 0 to 20 min (Δ20) and from 0 to 50 min (Δ50), and NA from the preexercise to the post-exercise periods (Δ50) were correlated with the coefficient of variation of 100 successive R-R intervals during normal breathing (CVR-R).
Thereafter two groups were selected (group A: CVR-R<2%, n=7, Group B: CVR-R 2%, n=9). Age, body mass index (BMI) and absolute work load (watt) did not differ between the groups. The levels of heart rate at 10 and 50 min after initiation of exercise, FFA at 50 min, cortisol at 20 min and NA during the post-exercise period were higher in group A. IRG levels were elevated at 20 and 50 min in group A but were unchanged in group B.
In NIDDM patients with decreased beat-to-beat variation in heart rate at rest, sympathetic responses to exercise are delayed and derangement of endocrine function may mean partial compensation for mobilizing energy substrates during exercise. The delayed hyper-responses of catecholamines may be related to cardiac arrest or high mortality reported in diabetics with autonomic neuropathy and to progression of vascular complications in diabetics.View full abstractDownload PDF (1128K) -
Yutaka Mori, Matsunobu Suko, Hirokazu Okudaira, Ikuro Matsuba, Akira T ...1987 Volume 30 Issue 2 Pages 113-119
Published: February 28, 1987
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSThe adoptive transfer of spleen cells from Cyclosporin-treated NOD mice was performed to investigate the involvement of suppressor T cells in the preventive effect of Cyclosporin on insulitis in NOD mice.
The donor spleen cells were obtained from female NOD mice with acute diabetes (Group I), Group I + Cyclosporin-treated (25 mg / kg/2 days for 40 days) female NOD mice aged 100 days (Group II), Group I + Cyclosporin-treated (25 mg/kg/2 days for 40 days) female NOD mice aged over 240 days (Group III), and female NOD mice aged 30 days (Group IV). The recipients of all groups were female NOD mice aged 30 days. Plasma glucose was measured every week, and 4 weeks after the transfer the pancreases were examined for histological changes. There was no significant difference in the plasma glucose levels in any group throughout the experiment. When the intensity of insulitis was graded 0 to 3, the intensity of insulitis in Groups I and III was reinforced significantly more than that in Group IV and the development of insulitis in Group II was more significantly suppressed than that in Group I.
1) The adoptive transfer of spleen cells from old NOD mice with acute diabetes accelerated the development of insulitis in young NOD mice, without inducing hyperglycemia. 2) The additional adoptive transfer of spleen cells from Cyclosporin-treated NOD mice decreased the acceleration of development of insulitis observed in young NOD mice which received spleen cells alone from old NOD mice with acute diabetes. 3) This effect was not demonstrated in the experiments where Cyclopsporin-treated mice aged over 240 days were used as donor.
These results indicate that active suppressor mechanisms are involved in the preventive effect of Cyclosporin on insulitis in NOD mice.View full abstractDownload PDF (3201K) -
Haruhiko Isotani, Akito Kitazawa, Haruko Kitaoka, Youichi Ikegami, Tak ...1987 Volume 30 Issue 2 Pages 121-126
Published: February 28, 1987
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSA preliminary multivariate analysis in patients with diabetes mellitus (n=109) between urinary excretion of N-acetyl-β-D-glucosaminidase (u-NAG) and nine parameters including age, duration, HbA1c, concentrations of plasma glucose, BUN, creatinine, β2-microglobulin in a fasting state, degree of proteinuria and degree of retinopathy was performed, and changes of u-NAG levels showed a close correlation with the changes of HbA1c, as well as with age and the degree of proteinuria.
From this data, further study on patients with diabetes mellitus (n=84) was undertaken to investigate changes of u-NAG levels in relation to changes of HbAic during the course of treatment. Levels of u-NAG in 10 patients with uncontrolled hyperglycemia were 14.9±7.0 U/g. creat (mean±SD), and decreased in all to 8.0±3.9 U/g. creat two months after hyperglycemia was corrected by the administration of insulin or an oral hypoglycemic agent. U-NAG levels significantly increased from 7.1 ± 2.6 U/g. creat to 12.1 ±4.9 U/g. creat in another group of 10 diabetic patients whose glycemic control worsened in two months, as seen by the increase in HbA1c from 7.3 ± 0.8% to 9.1 ±0.9%. On the contrary, in 64 patients whose HbA1c did not show a remarkable change, u-NAG levels also had no changes.
To examine when u-NAG levels start to the affected by the change of plasma glucose levels, u-NAG was serially measured, in 15 patients who were admitted to our hospital. In 10 of them, hyperglycemia improved within a week, and their levels of u-NAG decreased significantly at four weeks after euglycemia was achieved. In the remaining five patients whose hyperglycemia did not improve within a week, u-NAG levels did not show a significant decrease.
Transient hyperglycemia induced by the 75 g oral glucose load test brought about no increases in u-NAG levels.
These results suggest that urinary excretion of NAG is closely related to the glycemic control in patients with diabetes mellitus.View full abstractDownload PDF (942K) -
Masahiro Tsutsui, Tomio Onuma, Shigeru Ochiai, Akitoshi Boku, Takashi ...1987 Volume 30 Issue 2 Pages 127-132
Published: February 28, 1987
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSVitamin E levels of platelets and plasma were measured fluorometrically in 72 type 2 diabetics (mean age, 59 years) and 30 healthy controls (mean age, 57 years). Vitamin E levels of the platelets were 0.85 ± 0.05 μg/109 platelets (mean ± SE) in the diabetics. This was significantly higher than the value of 0.53 ± 0.03μg/109 platelets in healthy controls (p<0.001). Vitamin E levels of plasma in diabetics were 1.14 ± 0.04 mg/dl, also significantly higher than that in healthy controls (0.91 ± 0.03 mg/dl)(p<0.001). There was a positive correlation between vitamin E levels of platelets and of plasma in diabetics (r=-0.336, p<0.01).
The correlation between diabetic vascular complications and vitamin E levels of platelets was studied in diabetics. Vitamin E levels of platelet in the patients with proteinuria (1.14 ±0.19 μg/109 platelets) was significantly higher than that in the patients without proteinuria (0.77 ± 0.04 μg/109 platelets)(p<0.01). Among the patients with proteinuria, vitamin E levels of platelets in the patients with ischemic coronary disease (0.62 ± 0.08μg/109 platelets) were significantly lower than in the patients without ischemic coronary disease (1.40±0.24μg/109 platelets)(p<0.05).View full abstractDownload PDF (898K) -
Analysis Using the Insulin-sensitive Phosphodiesterase Activation SysternTakashi Suzuki, Hideichi Makino, Azuma Kanatsuka, Sho Yoshida1987 Volume 30 Issue 2 Pages 133-139
Published: February 28, 1987
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSThe effects of various concentrations of trypsin on insulin-sensitive phosphodiesterase activity and insulin binding in isolated fat cells were investigated. The cells were treated at the lowest tracer insulin concentration (0.08 nM), at 24°C for 60 min. The specific binding of radioactive insulin to fat cells treated respective by with none, 10 μg/ml and 1 mg/ml of trypsin was 4.8%, 4.0% and 0.4%/2 × 105 cells. Scatchard analysis indicated a decrease in the number of insulin receptors in fat cells treated with trypsin.
To measure the phosphodiesterase activity, isolated fat cells were treated with none, 10 μg/ml and 1 mg/ml trypsin at 37°C for 15 min, then incubated at 37°C for 10 min with or without insulin. A crude microsomal fraction prepared by differential centrifugation was assayed for the phosphodiesterase activity. In all but the basal activity, the enzyme activity in trypsin-treated fat cells was lower at all insulin concentrations. In fat cells treated with 10 μg/ml of trypsin, the dose-response curve of the phosphodiesterase activation by insulin shifted to the right, and half-maximum stimulation was obtained at 0.43 nM compared with 0.15 nM insulin concentration in the controls (p<0.001). This indicates a decrease in sensitivity to insulin. Responsiveness to insulin, expressed as a percentage of the basal enzyme activity, was also reuced to 200% in fat cells treated with 10 μg/ml of trypsin, compared with 260% in the controls (p<0.001). In fat cells treated with 1 mg/ml of trypsin, the phosphodiesterase activation by insulin disappeared.
These results indicate that changes in the binding of insulin to its specific receptors directly affect the subsequent biological action of insulin.View full abstractDownload PDF (957K) -
Takehiko Majima, Akito Kitazawa, Haruko Kitaoka, Youichi Ikegami, Haru ...1987 Volume 30 Issue 2 Pages 141-145
Published: February 28, 1987
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSWe have investigated the effects of Gliclazide and Glibenclamide on glycemic control in 20 Type II diabetics. All patients were treated with a daily single dose of Glibenclamide 2.5-5.0 mg and were kept under stable glycemic control for 4 months. Using an equivalent tablet for tablet dose, the patients were then switched to Gliclazide. Each patient was seen monthly for 8 months, and the fasting plasma glucose levels (FPG), HbA1 and HbA1c were recorded.
During the Glibenclamide period, the patients' mean FPG (±SD) was 146±21 mg/dl. Switching to Gliclazide produced a significant increase in mean FPG (157 mg/dl, after one month and 170 mg/dl, after 4 months). But the HbA1 and HbAic did not change significantly throughout the observation periods. After the switch to Gliclazide, the FPG increased in 9 of the 20 patients (> 10 mg/dl) but the HbA1c increased in 4 patients (> 0.5%) and decreased in 5 patients (>0.5%).
Although there is some evidence that a pharmacological difference between the 2 drug exists, our conclusion is that the hypoglycemic effects of Glibenclamide of 2.5 mg are equal to Gliclazide at 40 mg.View full abstractDownload PDF (619K) -
Masako Waki, Hideki Koh1987 Volume 30 Issue 2 Pages 147-154
Published: February 28, 1987
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSNoradrenaline (NA) levels in the circulation is considered to reflect sympathetic nervous activity in humans. This study was conducted to clarify the NA response to glucose ingestion (75 g) in ten non-insulin-dependent diabetic inpatients (NIDDM) and eight inpatients with normal glucose tolerance free from autonomic disturbances (controls).
Venous blood samples were withdrawn at 30-min intervals for 2 h and at 60-min interval for 1 h to determine plasma glucose, serum NEFA, IRI, CPR, potassium, NA and adrenaline levels. The following results were obtained:
1) In the controls, the maximum increase in serum NA levels occurred at 30 min after glucose ingestion, but in the diabetics, the mean serum NA levels remained unchanged.
The effects of glucose ingestion were significantly different between diabetics and controls according to the analysis of variance for serum NA levels (p<0.05).
2) In the total group (n=18), positive correlations were found between 4 NA 30 min and ΔIRI 30min (r=0.52, P<0.05), between %ΔNA 30min and ΔIRI 30min (r=0.56, P<0.05), bctween ΔNA 30min and ΔIRI/Δ Glucose ratio (insulinogcnic index)(r=0.70, P<0.01), and between %ΔNA 30min and ΔIRI/ΔGlucose ratio (r=0.69, p<0.01).
3) In four diabetics, NA responses to glucose ingestion were studied again after caloric restriction for 2 weeks. In three of them, both the NA response and the IRI response to glucose ingestion were improved after diet therapy, but in the remainder, the NA response to glucose ingestion remained unchanged in accordance with the sustained poor insulin response to glucose ingestion.
In conclusion, it appears that the NA response to glucose ingestion is regulated primarily by the insulin response to glucose ingestion, and the impairment of the NA response to glucose ingestion constitutes one of the etiologic factors for the development of autonomic disturbances or metabolic derangement in NIDDM.View full abstractDownload PDF (941K) -
Shunji Hoshiyama, Katsunori Nao, Nobuyuki Ueda, Masashi Kubota, Misako ...1987 Volume 30 Issue 2 Pages 155-160
Published: February 28, 1987
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSTo evaluate the efficacy of the essential amino acids (EAA) on diabetic renal failure, 18 diabetic patients associated with renal failure were studied retrospectively and divided into the following 3 groups; 1) EAA-nontreated group (n=6), 2) EAA-effective group (n=4), 3) EAA-noneffective group (n=8). Their ages and duration of diabetes were mutually comparable. EAA supplementation consisted of 6.3-12.6g of oral or intravenously administered EAA, accompanied by a diet including 40-50g of protein and 1, 500-1, 800 calories a day.
Comparison of clinical data at the start of the EAA therapy revealed significant differences only in BUN and serum creatinine (SCr) between the EAA-effective and-noneffective groups. The level of BUN and SCr were 53±13.6 mg/dl and 3.6±1.3 mg/dl in EAA-effective group. In EAA-noneffective group the respective levels were 69±7.1 mg/dl and 6.9±1.9 mg/dl.
The progression of renal failure in the 3 groups was analyzed by comparing the slopes of the regression lines of the reciprocal of SCr (1/SCr) over time. After EAA therapy, the slope of the regression line became significantly less in the EAA-effective group but not in the EAA-noneffective and-nontreated groups. However 2 years prior to EAA therapy in the EAA-noneffectivc group and at 2 years prior to the stage of SCr over 5.0 mg/dl in EAA-nontreatcd group the 1/SCr slope In as less than 0.5, but in the EAA-effective group it was more than 0.5.
These results indicate that EAA therapy is no longer effective for diabetic renal failure after the SCr exceeds 5.0 mg/dl, and that EAA therapy may be initiated when SCr exceeds 2.0 mg/dl to alleviate the progression of diabetic renal failurcView full abstractDownload PDF (959K) -
Relationship between Kidney Size and Diabetic Rena Lesion in Non-insulin-dependent Diabetes MellitusShigeki Inomata, Masanori Inoue, Yoshiyuki Oosawa, Masuo Itoh, Osamu M ...1987 Volume 30 Issue 2 Pages 161-166
Published: February 28, 1987
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSThe purpose of this study was to determine the relationship between kidney size and diabetic renal lesion in non-insulin-dependent diabetes mellitus (NIDDM). Kidney size was measured in 22 normal controls and 67 diabetic patients (9 cases with persistent proteinuria, 36 cases with retinopathy) and was expressed as the renal ratio determined by the method of Simon using intravenous pyelograms. Renal biopsy was performed in 19 diabetics and diabetic glomerular diffuse lesion was graded into four classes based on Gellman's classification.
The following results were obtained;
1) The renal ratio was significantly larger in diabetic patients than in the controls (p<0.01).
2) Based on renal ratio in the controls, the diabetics were subdivided into S (mean-SD≥) M (mean-SD-mean+SD) and L (mean+SD ≤) groups. Cases of diabetics belonging to the S, M and L groups were 4, 32 and 31 respectively. Persistent proteinuria was found in 0, 6.3 and 22.2% of the patients in the S, M and L group respectively.
3) In 19 diabetics whose kidneys were biopsied, glomerular diffuse lesion was grade I or II in all seven cases in the M group, and grade III or IV in six out of twelve cases in the L group. Kidneys with glomerular diffuse lesion of grade III or IV were significantly larger than those with glomerular diffuse lesion of grade I or II (p<0.05).
From these results, it was concluded that in the NIDDM risk of progression into persistent proteinuria was higher in patients with enlarged kidneys than in those without it.View full abstractDownload PDF (887K) -
Junko Fujimoto, Meisei Hirota, Michiko Hata, Mamiko Kondo, Kenji Shima1987 Volume 30 Issue 2 Pages 167-173
Published: February 28, 1987
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSAutonomic nerve functions were evaluated based on variations in the R-R interval in the electrocardiographs of 1, 261 healthy subjects from 5 to 79 years of age, and the normal reference ranges and standard prediction equations were derived. R-R intervals were recorded at rest, during deep breathing, during Valsalva manoeuvre, and on standing, and their mean, standard deviation (SD), coefficient of variation (CV), and the ratio of maximal to minimal value (MAX/MIN) were calculated. Age, but not sex, was significantly correlated with the parameters of autonomic nerve function. Therefore normal reference ranges obtained by a parametric method were subdivided into 8 levels by age in decades. SD, CV, and MAX/MIN of 100 R-R intervals at rest and during deep breathing significantly decreased (p<0.01) with aging. Moreover, the multiple correlation coefficient of autonomic nerve functions with the biological characteristic factors (sex, age, body weight, and height) were calculated, and standard prediction equations of high reliability (p<0.01) were obtained by multivariate analysis of the autonomic nerve functions.View full abstractDownload PDF (969K) -
Naoko Iwasaki, Hiroko Yoshino, Hiroshi Ohashi, Tadasu Kasahara, Yukima ...1987 Volume 30 Issue 2 Pages 175-180
Published: February 28, 1987
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSIt has been confirmed that diabetic microangiopathies are usually not progressive in Caucasian patients with maturity-onset type diabetes of the young (MODY). MODY is classified as noninsulin-dependent diabetes mellitus (NIDDM) characterized by a dominant heredity. The onset of the disease is before the age of 25 years.
However microangiopathies in Japanese patiens with MODY seem to be not so rare and in some the progression of the microangiopathies is rapid. A case of MODY with proliferative retinopathy and neuropathy was admitted our hospital in 1984.
At admission she was 30 years old. Diabetes was found when she was 11 years old and she was treated with diet alone for 9 years. When she was 20 years old, proliferative retinopathy appeared and insulin therapy was started at that time. Albuminuria occurred at the age of 26 years, and elevation of the serum creatinine level at the age of 28 years.
Her mother, 56 years old, also suffers from diabetic proliferative retinopathy and receives hemodialysis for diabetic nephropathy. The mother's diabetes was found 40 years ago and her father was also diabetic from the age of 30 years.
A younger sister, now 28 years old, had diabetes with retinopathy when she was 17 years old. The retinopathy is now proliferative and intermittent albuminuria is present.
In conclusion, the female patient reported in this paper became diabetic before 25 years of age and have a dominant heredity of NIDDM with rapid onset and progression of microangiopathies.View full abstractDownload PDF (3129K) -
Kaoru Inoue, Taro Wasada, Mizuho Nakagawa, Akihiko Tazoe, Hiroshi Ono, ...1987 Volume 30 Issue 2 Pages 181-185
Published: February 28, 1987
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSA 55 year-old woman, who had had diabetes for 2 years, was admitted to our hospital because of marked emaciation (body mass index 13.6) and painful neuropathy. She was chronically ill and apathetic. With daily insulin treatment (14-16 U), her fasting blood glucose was 150 mg/dl and HbA1 9.6%. Renal and endocrine functions including the thyoid gland, the pituitary adrenocortical axis and the renin aldosterone system were normal. She had the clinical features of severe symmetric peripheral neuropathy. The MCV of posterior tibial nerve was 32.4 m/sec. The SCV of the sural nerve could not be evoked. The R-R interval variation during deep breathing was 2.3 beats/min. Biopsy of the sural nerve revealed a marked loss of both myelinated and unmyelinated nerve fibers, independent of fiber size. Her blood showed low Na concentrations (127-131 mEq/l) and hypo-osmolarity (236-256 mOsm/l). Water loading (20 ml/kg) failed to dilute the urine below the level of the plasma osmolarity and the plasma ADH was not significantly suppressed. Urinary Na output was relatively large (28-120 mEq /l) in the presence of hyponatremia. Interestingly, these abnormalities in the water loading test persisted for 2 months after discontinuation of treatment with carbamazepine, when serum Na had already been normalized. These findings suggest that a certain causal linkage may exist between inappropriate secretion of ADH and severe diabetic neuropathy.View full abstractDownload PDF (794K) -
Narihito Yoshioka, Yasuhiko Iwamoto, Ayako Matsuda, Takeshi Kuzuya1987 Volume 30 Issue 2 Pages 187-189
Published: February 28, 1987
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSA specific and simple radioimmunoassay was developed for human proinsulin. Antiserum against human proinsulin was produced in guinea pigs immunized with an emulsion of antigen and Freund's adjuvant. Only one out of six guinea pigs produced proinsulin-specific antiserum that did not crossreact with human insulin or C-peptide. A double antibody method, using anti-guinea pig γ-globulin rabbit serum as a second antibody, was used to separate bound and free 125I-proinsulin in the reaction mixture. With this radioimmunoassay, it was possible to quantify directly without extracion 0.003 pmol/ml of circulating human proinsulinin serum. The mid-range (IC 50) of the assay was 0.075 pmol/ml. The mean intra-and interassay coefficients of variation were 5.5% and 9.8%. The recoveries of proinsulin added to serum were in the range 92-119%. The normal fasting proinsulin level in serum was 0.008±0.003pmol/ml, increasing gradually after a 100-g oral glucose load, and reached a peak level of 0.021±0.006 pmol/ml after 120 min.View full abstractDownload PDF (420K)
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