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Volume 19, Issue 3
Displaying 1-21 of 21 articles from this issue
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Yasuo Goto, Yutaka Seino, Tomohiko Taminato, Masaki Ikeda, Hiroyuki Ku ...1976 Volume 19 Issue 3 Pages 277-284
Published: May 31, 1976
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSAlthough arginine-induced hyperglucagonemia has been observed in diabetics and in patients with Cushing's syndrome or hypothyroidism, the influence of treatment on arginine-stimulated glucagon levels in these diseases is still obscure. In the present study, in order to throw some light on this problem, arginine-induced glucagon levels in these diseases were examined before and after treatment.
In diabetics, the hyperresponse of glucagon to arginine was significantly decreased by treatment with insulin or sulfonylureas. However, glucagon levels after treatment were found to be still relatively excessive with respect to concomitant glucose levels.
Excessive glucagon response to arginine as observed in Cushing's syndrome was normalized after adrenalectomy.
In the case of hypothyroidism excessive glucagon response to arginine was also normalized with treatment.
These results suggest that abnormal glucagon secretion seems to play a significant role in the pathogenesis of diabetes mellitus. But this could be partially due to the consequences of the disordered metabolic state induced by the lack of insulin. On the other hand, arginine-induced hyperglucagonemia found in patients with Cushing's syndrome or hypothyroidism may be a simple consequence of the disturbed metabolic state of these diseases.View full abstractDownload PDF (1128K) -
Yasuhiko Matsuura, Yasuo Morimoto, Toshio Obayashi, Hiroshi Saitoh, Yo ...1976 Volume 19 Issue 3 Pages 285-289
Published: May 31, 1976
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSCyproheptadine administration has been demonstrated to stimulate appetite. Our previous report demonstrated a depression of blood glucose by cyproheptadine irrespective of circulating insulin level in rats.
The aim of the present study is to determine the effect of cyproheptadine on blood glucose, serum insulin and serum growth hormone level during, 1) the standard oral glucose tolerance test (OGTT), and during 2) the intravenous glucose tolerance test (IVGTT).
The subjects were seven apparently healthy males without family history of diabetes, aged from 23 to 25. Blood samples were drawn from the cubital vein before, and 30, 60, 90, and 120 minutes after oral administration of 50g of glucose.
In IVGTT, blood samples were collected before and at 3, 5, 7, 10 minutes and after every ten minute interval until 60 minutes.
Time was counted zero at the start of the intravenous injection of 10 g of glucose in 50% aqueous solution.
After examining all seven subjects with OGTT and IVGTT to obtain control values, cyproheptadine 8mg per day in tablet form, was administered for seven to ten days until the other OGTT and IVGTT were completed. Results obtained are as follows.
Blood glucose levels in subjects under cyproheptadine treatment during OGTT were lower than those of controls. Differences of glucose levels were significant in 60 minutes and 90 minutes during OGTT.
Changes in insulin levels, however, in OGTT after administration of cyproheptadine were minimum. 5 subjects on cyproheptadine had serum growth hormone levels lower than the controls in OGTT, but the differences were not significant.
In IVGTT cyproheptadine had no effect on serum insulin levels.
However, glucose disappearance ratio (K-value) in IVGTT was 1.7±0.1 for the control and 2.6±0.4 for cases with cyproheptadine treatment (p<0.05). These results in combination with our previous report may indicate enhancement of blood glucose utilisation in peripheral tissues irrespective of change in circulating insulin levels in man.
The next suggestion from the present study is that cyproheptadine has no effect on the insulin secretory response of the B cell of the islet of Langerhans during IVGTT in which the effect of the gut factor is neglected and insulinogenesis is a result of a direct hyperglycemic stimulus on the B cell.View full abstractDownload PDF (616K) -
Yoshiro Shioda, Akio Ueda, Minoru Matsuzaki, Teiji Arita, Masako Horii ...1976 Volume 19 Issue 3 Pages 290-296
Published: May 31, 1976
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSSerum proteins, particularly complements such as β1-C / A-globulin (β1C / A) and β1-E-globulin (β1E), proteinase inhibitors such as α1-Antitrypsin (α1AT), α1-Antichymotrypsin (α1X), Inter-α-Trypsininhibitor (IαI), α2-Macroglobulin (α2M), and Antithrombin III (AthIII), and other glycoproteins such as α1-Acid-Glycoprotein (α1AG), Ceruloplasmin (Cp), Haptoglobin (Hp), and Transferrin (Tf) were quantitatively measured by the use of the single radial immunodiffusion method in 122 cases of diabetes mellitus and in 23 normal adults (group H).
Diabetic patients were divided into three groups, group D: 44 diabetics without clinical mannifestations of microangiopathy, group R: 61 diabetics with retinopathy, and group N: 17 diabetics with nephropathy.
The results are summarized in the following. (1) In group D, increase of both β1C/A and β1E and decrease of AthIII were observed. (2) In group R, an increase of α2M was observed in addition to the changes found in group D. (3) In group N, tendency of α1AG to increase, a significant increase of α1AT, and a remarkable increase of α2M were observed in addition to the changes found in other two groups. (4) In patients being treated with insulin, increase ofα2M was demonstrated with seemed to become more pronounced as the involvement of microangiopathy progressed.
As these serum proteins, the changes of which were observed in our study, are mostly closely related to the coagulation and fibrinolysis systems of the blood, it is suggested that changes of these serum proteins in diabetic patients would reflect one of the clues to elucidate the pathogenesis of diabetic microangiopathy, and that diabetic patients showing remarkable changes of these serum proteins might need careful clinical management in order to prevent progression of microangiopathy.View full abstractDownload PDF (988K) -
Aritoshi Sakamoto, Yutaka Harano, Noboru Araki, Kanji Izumi, Yasuhisa ...1976 Volume 19 Issue 3 Pages 297-303
Published: May 31, 1976
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSOral maltose tolerance tests (50g or 100g) were performed on normal subjects, diabetics, and subjects with impaired exocrine function of the pancreas. The blood sugar and IRI-responses were compared with those obtained by glucose, liquid glucose or starch tolerance tests. In normal and diabetic subjects, blood sugar and IRI-responses were almost identical in both maltose and glucose tolerance tests. Therefore, maltose tolerance tests can be judged by the same criteria as glucose tolerance tests.
However, in subjects with obstruction of the pancreatic duct or with external pancreatic drainage, hyperglycemic effect is more marked in cases receiving maltose than in those receiving an equivalent amount of liquid glucose or starch. Thus, in 4 cases, maltose tolerance test results were diabetic in contrast to “borderline” according to liquid glucose test. In a patient with chronic pancreatitis who has a low amylase output, the borderline diabetic curve by liquid glucose tolerance test was turned out to be diabetic by the maltose tolerance test.
The results indicate that maltose has less abdominal side effect than glucose and seems more sensitive than liquid glucose for the diagnosis of diabetes mellitus in cases with abnormal exocrine function of the pancreas. Since maltose is a physiological digestive end-product of the carbohydrate in the intestinal lumen and is absorbed as rapidly as glucose, it is thought to be an ideal substance for oral glucose tolerance tests.View full abstractDownload PDF (924K) -
Kenji Shima, Suzue Morishita, Katsunori Ishikawa, Norio Sawazaki, Kiku ...1976 Volume 19 Issue 3 Pages 304-312
Published: May 31, 1976
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSIn order to investigate the pancreatic β-cell function in insulin-treated diabetics and in a patient with insulin-autoimmune disease in whom a direct measurement of IRI is impossible because of the presence of an insulin antibody in their sera, the concentration of CPR (C-peptide immunor-eactivity) was determined during the oral glucose tolerance test in 40 insulin-treated diabetics (D2 & D3) and the patient with insulin-autoimmune disease (I. A.). These results were compared with those of 6 normal subjects (N), 4 obese patients (O) and 10 newly diagnosed diabetics (D1).
According to the reactivity of their β-cell to glucose the patients treated with insulin were divided into two groups: 32 responder (D2) and 8 non-responder (D3). The mean fasting and peak levels of CPR in these groups are as follows:
N: 1.37 ± 0.77 and 5.05 ± 1.09 mμg/ml,
O: 5.04 ± 1.11 and 13.2 ± 4.88 mμg/ml,
D1: 3.75 ± 0.79 and 10.2 ± 3.58 mμg/ml,
D2: 2.92 ± 1.58 and 5.33 ± 2.86 mμg/ml,
D3: 0.77 ± 0.53 mμg/ml and no noticeable peak,
I. A.: 38.0 and 49.6 mμg/ml.
The CPR values obtained from N, O and D1 during OGTT were positively correlated with immunoreactive insulin levels. When the sera of high CPR values containing insulin antibodies were acidified and gel-filtered it was revealed that a main component of CPR was proinsulin. In 10 insulin-treated juvenile diabetics only 4 patients were non-responders. Residual β-cell secretory capacity is thus present in many insulin-treated juvenile diabetics.
The relationship between residual β-cell secretory capacity and the metabolic stability of diabetic patients is discussed.View full abstractDownload PDF (1531K) -
Tokutaro Sato, Keigo Yasuda, Tsuyoshi Saito, Kaoru Yoshinaga1976 Volume 19 Issue 3 Pages 313-317
Published: May 31, 1976
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSThe effect of insulin (90 units), or chlorpropamide (250-500 mg) and buformin (150 mg) on blood glucose and plasma lipids were studied in 2 cases of lipoatrophic diabetes.
Neither insulin nor oral agents could control the blood sugar or plasma lipids, but elevated them, especially plasma triglyceride.
Furthermore, abrupt withdrawal of insulin or oral agents did not make diabetes worse, but decreased blood glucose and plasma triglyceride. The degree of hepatomegaly also decreased after withdrawal of insulin or oral agents.
The effects of 3 kinds of isocaloric diet of 1200 cal with 23 g of fat and different amounts of protein and carbohydrate were also studied in one case of lipoatrophic diabetes.
(On the high protein diet with 100 g of protein and 148 g of carbohydrate as well as on the diet with 85 g of protein and 163 g of carbohydrate, the patient complained of anorexia and fatigue accompanied by an increment of plasma triglyceride.) On the other hand, a well-balanced diet with 58 g of protein and 190 g of carbohydrate reduced both blood glucose and plasma triglyceride.
It was concluded that restriction of calorie intake with a well-balanced diet is essential for the treat ment of lipoatrophic diabetes, and that neither, insulin nor oral agents are effective.View full abstractDownload PDF (697K) -
The Levels of Glycolytic Intermediates in Leg Muscles with or without Electrical Stimulation, and the Levels of Activity of Some EnzymesMitsuo Imura1976 Volume 19 Issue 3 Pages 318-326
Published: May 31, 1976
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSThe changes in levels of glycolytic intermediates of leg muscles were studied in vivo on 4 groups of rats: the conrol, the insulin-administered, the streptozotocin-diabetic, and the insulinadministered diabetic group. Activities of some glycolytic enzymes in the muscles of the 4 groups were assayed.
1) In the diabetic group without the electrical stimulation, levels of glycogen and lactate were increased about 1.5-fold, but those of other glycolytic intermediates were not changed. Activities of phosphofructokinase, pyruvate kinase, and lactate dehydrogenase were not affected by inducing diabetes, but the pyruvate dehydrogenase complex was decreased. Activities of the pyruvate dehydrogenase complex were restored by insulin administration.
2) In both insulin-administered groups, levels of glycolytic intermediates (except the increase in glucose 1-phosphate, glucose 6-phosphate and lactate) were unchanged. Activities of key enzymes in glycolysis also remained constant.
3) In all of the 4 groups, the electrical stimulation resulted in a decrease in the glycogen level and the increase in levels of some glycolytic intermediates. There was no difference among the groups in metabolic changes by the electrical stimulation.
It is concluded that the metabolic steps from glucose 6-phosphate to pyruvate in the skeletal muscle of the diabetic rat is not affected, but the step catalyzed by the pyruvate dehydrogenase complex is supressed, and that the enhancement of glycolysis by insulin administration is not accompanied by an increase in the quantities of glycolytic key enzymes.View full abstractDownload PDF (1630K) -
Hidetaka Nakayama, Takashi Sasaki, Takuji Watanabe, Kouichi Yoshino, M ...1976 Volume 19 Issue 3 Pages 327-333
Published: May 31, 1976
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSStudies were undertaken to examine cholesterogenesis in the intestine of streptozotocin diabetic rats by measuring incorporation of [2-14C] acetate into cholesterol and 3-Hydroxy-3-methylglutaryl CoA reductase (HMG-CoA reductase, EC 1. 1. 1. 34) activity. In these diabetic rats, the intestinal mucosal wet weight and the food consumption were markedly increased. Serum insulin levels in these diabetic rats decreased at both noon and midnight. Serum total cholesterol levels were slightly but significantly increased in these diabetic rats. The incorporation of [2-14C] acetate into cholesterol was significantly increased in all diabetic intestinal segments. In addition, the jejunal-ileal gradient in the intestinal cholesterogenesis persisted in the diabetic intestine. On the other hand, it did not affect the rate of fatty acids or carbon dioxide production except in the jejunum. Hepatic HMG-CoA reductase activities were markedly reduced at both noon and midnight in these diabetic rats. The diurnal variation appeared to be nearly abolished. In contrast, the specific activities of this enzyme in the jejunal crypt layer at both noon and midnight were significantly increased in these diabetic rats. In addition, the diurnal variation was observed in the diabetic jejunal crypt layer. Also, total reductase activity per segment in the jejunal and ileal mucosa (villi +crypt layer) was increased in these diabetic rats. The jejunal-ileal gradient in the total reductase activity did not change significantly with streptozotocin diabetes.
The results indicate that in the streptozotocin diabetic rat a marked decrease in cholesterogenesis occurs in the liver, whereas an increase in cholesterogenesis occurs with diurnal variation in the intestine.View full abstractDownload PDF (1143K) -
Hidehiro Hashimoto1976 Volume 19 Issue 3 Pages 334-343
Published: May 31, 1976
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSDiabetic patients were divided into four groups: those without vascular complications (M), those with nephro-and retinopathy (P), those with ischemic heart disease (I), and those with hypertension (H). Serum levels of α2-Macroglobulin (α2-M), total cholesterol, triglycerid, free fatty acid, β-lipoprotein, fasting blood sugar and blood fibrinolytic activity were determined and compared with the values obtained in normal controls (N)
.α2-M was higher in groups P and I than in groups N, M or H with a statistical significance, while no difference was found in any pair of groups N, M and H. The fasting blood sugar was high in group P, showing a statistically significant correlation with α2-M. Lipid levels were significantly higher in every group of diabetics, but the increase of α2-M was more marked than that of lipids in group P, while the opposite relationships were observed in groups M, I and H. As to the fibrinolytic activity, fibrinogen was significantly higher in group P than in N or M, and relatively higher values were observed in groups H and I. The fibrin plate lysis area with a mixture of euglobulin and streptokinase showed lower values in every group of diabetics than in the normal control, but the relationships between α2-M and the fibrinogen level or lysis area in group P was no different from those in other groups. No difference was revealed in the euglobulin lysis time. These results indicate the existence of a very close relationship between α2-M and nephro-and retinopathy. It is suggested that if blood α2-M promotes the development of nephro-and retinopathy, α2-M would exert its influence not only through its antiplasmin effect but also directly on the development of nephro-and retinopathy. At any rate, the differents behaviors between micro-and macroangiopathy regarding the serum α2-M level suggests that these two kinds of vascular lesions have different developmental mechanisms.View full abstractDownload PDF (1637K) -
Kazuhisa Komura, Yoshio Kodama, Mitsuo Ito, Yoshihiro Nakamura, Seibei ...1976 Volume 19 Issue 3 Pages 344-352
Published: May 31, 1976
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSThe cause of death of 603 diabetics between January 1972 and December 1973 in university hospitals, public hospitals and private hospitals, was studied and the following results were obtained.
1) Because these cases were obtained in three different types of hospitals, it is presumed that there may be a little bias than in previously published reports.
2) Of the 603 cases, 488 cases were primary diabetes.
Since autopsies were performed in only 81 cases, the rate of autopsy was found to be 13.4 per cent. Therefore, the classification of the cause of death is based upon the clinicai diagnosis when there was no autopsy.
3) It is of note that there were more deaths due to cerebrovascular accidens and fewer deaths due to neoplasms in private hospitals than in university hospitals.
On the other hand there were more cases of cardiac disease and diabetic coma in public hospitals, while in the university hospitals more deaths due to malignant neoplasm and fewer deaths due to cerebrovascular accident and diabetic coma were seen.
4) The leading causes of death were cerebrovascular accident (17.4%), renal disease (16.8%) and cardiac disease (16.8%), followed by malignant neoplasm (13.9%), infection (including tuberculosis)(12.7%) and diabetic coma (9.0%). Thus, the deaths from the cardiovascular disease including cardiac disease, renal disease and cerebrovascular accident made up about one half (51.8%) of the deaths among the diabetics.View full abstractDownload PDF (1388K) -
Naruto Horiuchi, Akira Sasaki, Takaichiro Suzuki, Yoshihiko Endo, Goic ...1976 Volume 19 Issue 3 Pages 353-359
Published: May 31, 1976
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSThe Alström syndrome is a hereditary disease associated with retinopathy pigmentosa, diabetes mellitus, obesity, and severe nerve deafness, which has been reported by Alström as an independent disease unit. This syndrome is very similar to the Laurence-Moon-Biedl syndrome, but can be differentiated from it by the association of diabetes mellitus, nerve deafness and lack of polydactyly, and mental retardation.
We experienced a female case of the Alström syndrome having cirrhosis of the liver in addition to retinopathy pigmentosa, diabetes mellitus, obesity and severe nerve deafness. The patient was a 25 year-old female, having a consanguineous marriage among her ancestors.
The disturbance of visual acuity began when she was three years old, and the hearing difficulty when she was five years old. She had been obese since her primary school age, and was diagnosed as diabetes mellitus at the age of seventeen.
Her first admission was when she was 22 years old. At that time, the fasting blood sugar was 156 mg/100 ml, serum cholesterol 233 mg/100 ml, serum triglycerides 252 mg/100 ml.The renal function was normal: The ophthalmological findings were heredo-macular dystrophy (Stargardt's disease) and pigmentary dystrophy with no pigment, and the otological finding was severe nerve deafness. A diagnosis of cirrhosis of the liver was made on the basis of laparoscopic examination and liver biopsy. No polydactyly, mental retardation or chromosomal abnormality was noted. The serum IRI level was high at fasting and increased markedly after glucose loading.
Although the dietary treatment was not always successful and sometimes the control of the diabetes mellitus was poor, a relatively small amount of insulin was effective in improving the diabetic symptoms. The liver and spleen became gradually enlarged. Finally she died suddenly from alimentary canal bleeding at the age of 25 years.
This case was discussed, comparing it with the case reported by Ikeda et al. as the first case of the Alström syndrome in Japan, and differentiating it from the Laurence-Moon-Biedl syndrome.View full abstractDownload PDF (4694K) -
Yasue Ohmori1976 Volume 19 Issue 3 Pages 360-368
Published: May 31, 1976
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSAlthough the binding sites to insulin in the human placental membranes have been recognized, the degradation of the insulin bound to them has not yet been elucidated.
Therefore the degradation of 125I-insulin by human placental membranes obtained from mature placenta of normal pregnancies, and early stage placenta at the time of artificial abortion was studied.
Using washed membranes and unwashed membranes, the degradation of 1251-insulin was examined by means of rebinding assay, TCA precipitation, binding by anti-insulin antibody, and gelchromatography. The effects of incubation time, temperature, and various concentrations of membranes were also investigated.
The results show that 125 I-insulin was degraded more by unwashed membranes, though the specific binding of unwashed membranes for 125 I-insulin was lower than that of washed membranes.
The degradation of 125 I-insulin depends on incubation time, temperature, and concentration of membranes, but it was not influenced by polypeptide hormones other than insulin.
While PCMB has no effect on the specific binding of 125I-insulin to membranes, 3 mM PCMB exhibited an inhibition of 125I-insulin degradation.
Although the specific binding of fetal placental membranes at early stage was lower than that of mature placental membranes, the 125 I-insulin degradation rates of fetal and mature placental membranes were same.
These results suggest that human placental membranes have both binding sites and a degradation system.View full abstractDownload PDF (1301K) -
[in Japanese]1976 Volume 19 Issue 3 Pages 369-377
Published: May 31, 1976
Released on J-STAGE: August 10, 2011
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[in Japanese], [in Japanese], [in Japanese], [in Japanese]1976 Volume 19 Issue 3 Pages 378-384
Published: May 31, 1976
Released on J-STAGE: August 10, 2011
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Taizo Hayashi, Haruo Yamaguchi, Shinichiro Nagai, Yoshikiyo Misugi, Sh ...1976 Volume 19 Issue 3 Pages 385-395
Published: May 31, 1976
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSIncreases of glucose excretion were observed in urine after 2 hours of a 40 g D-galactose tolerance test. At that time no more significant increase of blood glucose concentration was observed than in the control groups. Therefore, urinary glucose excretion after galactose loading was increased without the elevation of blood glucose levels. On the other hand some significant relationships were found between urinary glucose excretion and the elevation of blood galactose levels during galactose tolerance tests. Furthermore, the summation of stereoisomers, blood glucose, and galactose concentrations seemed to affect urinary glucose excretion and blood glucose threshold levels as a whole.
The monosaccharide transports in the kidney have been reported to be related to the stereospecificity of molecular structures. Following the interaction between glucose and galactose, galactose was absorped through the membrane in preference to glucose, and then glucose was excreted in urine. These findings suggest the necessity of chemical and steric studies on renal glycosuria.View full abstractDownload PDF (1495K) -
[in Japanese], [in Japanese], [in Japanese], [in Japanese], [in Japane ...1976 Volume 19 Issue 3 Pages 396-399
Published: May 31, 1976
Released on J-STAGE: August 10, 2011
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[in Japanese], [in Japanese], [in Japanese], [in Japanese]1976 Volume 19 Issue 3 Pages 400-403
Published: May 31, 1976
Released on J-STAGE: August 10, 2011
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Takayoshi Toyota, Kenichi Kimura, Mikihiko Kudo, Yoshio Goto, Kanji Ab ...1976 Volume 19 Issue 3 Pages 404-407
Published: May 31, 1976
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSA study was made on the insulin secretion of the perfused rat pancreas in response to a slowly rising glucose concentration. The pancreas with the proximal portion of the duodenum was removed from male Wistar rats (250-300g) by the modified method of Grodsky. The perfusate was a Krebs Ringer bicarbonate buffer containing 4.5% dextran (MW 60, 000). The flow rate was adjusted to 2 ml per min and the buffer was equilibrated in a mixed gas of 95%02 and 5 % CO2. When the glucose solution (1000 mg/100 ml) was added to the fluid reservoir (B in figure) containing 60 ml of 50 mg/100 ml glucose at a constant rate of 2 ml per min, the glucose concentration in the medium increased at a rate of 20 mg/100 ml per min. Insulin response to the slow-rise stimulus of glucose was divided into two phases. During the early phase (0-5 mim) the insulin secretion rapidly increased and in the late phase (15-20 min) it reached approximately the maximal level. When alprenolol (1.25μg/min), one of beta adrenergic blocking agents, had been added to the perfusate, the early phase of insulin secretion was not suppressed, but the late phase tended to be inhibited. Phlorizin (100μg/min) having a competitive inhibition of glucose transport through the cell membrane suppressed the early phase of insulin secretion, although the late phase of insulin response increased in phloridin addition. 2-deoxy-Dglucose (100μg/min) suppressed both the early phase and the late phase of insulin secretion in response to the slowly rising rate of glucose. The substances which inhibit insulin secretion act upon different sites of glucose transport and metabolism. These substances were shown to affect different inhibitory insulin responses to the slow-rise stimulus of glucose. The present experimental methods were useful to analyse the mechanism of insulin secretion.View full abstractDownload PDF (591K) -
Akira Kawa, Michio Nakazawa, Susumu Sakaguchi, Yasuko Kono, Hideo Haze ...1976 Volume 19 Issue 3 Pages 408-411
Published: May 31, 1976
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSFifty-seven Japanese diabetics were HLA typed with special reference to age at onset, insulindependency, and family history.
HLA-BW 22 was significantly more frequent in patients with juvenile onset, insulindependency, and/or with family history of diabetes mellitus than in controls. No difference, however, was found in the incidence of the phenotypes of HLA between controls and the patients with adult onset, insulin-independency or with negative family history. Thus, the inherited susceptibility to insulin-dependent diabetes seems to be associated with HLA-BW 22 in the Japanese, This finding might be another supportive evidence for the concept proposed by Nerup et al., that insulin dependent diabetes is a disease entity in itself and different from insulin-independent diabetes in etiology and pathogenesis. Our results showing the increase in BW 22, however, were different from those reported by Nerup et al. or Cudworth & Woodrow, who found a definite association of insulin-dependency or juvenile onset with HLA-B 8 and/or BW 15 in Caucasias. This difference seems to be an expression of race specificity in HLA phenotypes.
The interrelations among HLA, cellular immunity in diabetes mellitus, and virus infection as a possible cause of diabetes mellitus were also briefly discussed.View full abstractDownload PDF (629K) -
1976 Volume 19 Issue 3 Pages 423-433
Published: May 31, 1976
Released on J-STAGE: August 10, 2011
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1976 Volume 19 Issue 3 Pages 434-443
Published: May 31, 1976
Released on J-STAGE: August 10, 2011
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