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Volume 27, Issue 2
Displaying 1-9 of 9 articles from this issue
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Masashi Honda, Yasue Omori, Satomi Minei, Mayumi Sanaka, Keiko Azuma, ...1984 Volume 27 Issue 2 Pages 89-97
Published: February 29, 1984
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSDiabetic retinopathy worsens during pregnancy. To elucidate the exacerbating factors, platelet immunoreactive prostaglandin E (IRPG E) and plasma immunoreactive prostaglandin F2α (IRPG F2α) were assayed in pregnant diabetics.Eight pregnant diabetics and7nonpregnant diabetics were selected for the study.The control group consisted of8healthy nonpregnant nondiabetics and pregnant nondiabetics.There were3pregnant women whose retinopathy worsened from Scott 0to II during pregnancy.
The platelet IRPG E concentrations in the pregnant diabetics (7.9±4.0pg/105cell, Mean± SD) were significantly higher than those in the nonpregnant nondiabetics (3.9±1.7), pregnant nondiabetics (3.6±1.2) and nonpregnant diabetics (3.5±3.2).The plasma IRPG F2αconcentrations in the nonpregnant diabetics (3.5±0.8ng/ml) were significantly higher than those in the nonpregnant nondiabetics (2.1±0.9) and pregnant nondiabetics (1.6±0.4).The plasma IRPG F2α concentrations in the pregnant diabetics (7.0±4.8) were significantly higher than those in the nonpregnant nondiabetics and pregnant nondiabetics.The plasma IRPG F2αconcentrations in the pregnant diabetics were higher than those in the nonpregnant diabetics, but the difference was not statistically significant.Both the platelet IRPG E and plasma IRPG F2αconcentrations were the highest in the pregnant diabetics with retinopathy which worsened to Scott II stage during pregnancy.
These findings suggest that the platelet IRPG E and plasma IRPG F2αrepresented exacerbating factors of diabetic retinopathy during pregnancy.View full abstractDownload PDF (1078K) -
Naotaka Hashizume, Keiko Watanabe, Akiko Okada1984 Volume 27 Issue 2 Pages 99-105
Published: February 29, 1984
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSIn order to elucidate the mechanism of reproductive function disorders in diabetic rats, the frequency of estrous cycle abnormalities, the time relationships between estrous cycle abnormalities and onset of diabetes, and the hypothalamic, hypophyseal and ovarian functions in an alloxan diabetic condition were investigated using Wistar Imamichi mature male rats. Furthermore, the effects of insulin on the estrous cycle abnormalities were examined.
(1) Estrous cycle abnormalities were recognized in 75% of the diabetic rats, while no abnormality was recognized in the control group.
(2) The rates of occurrence of estrous cycle abnormalities were 40.5% between 5-10 days after onset of diabetes, 26.2% between 10-15 days, 19% between 15-20 days, 8.3% between 20-25 days, and 6% after 25 days.
(3) The ovary showed a reaction with administration of PMS-G. The hypophyseal reaction to LH-RH and the contents of LH and FSH were not different from those of the control group. There was also no difference in the hypothalamic LH-RH content as compared to that of the control group.
(4) Subcutaneous injection of 3 I.U. of Lent Insulin was carried out for 10 days, 24 hours after the administration of alloxan. During this period, estrous cycle abnormalities were not recognized but they appeared after discontinuation of the insulin. When insulin was administered to diabetic rats with continuous diestrous cycles, the estrous cycle recovered irrespective of the blood sugar values.
The above results suggest that the estrous cycle abnormalities of alloxan diabetes are different from those due to long-standing diabetes, such as retinopathy, renopathy and neuropathy, and that they occur at an early stage. Moreover, there were no abnormalities in the ovaries and hypophysis, although hypothalamic disorders were recognized. It was found that insulin is closely involved in such disorders.View full abstractDownload PDF (900K) -
Yutaka Tokumori, Isao Murakami, Akio Kurahashi, Satoru Kuno, Osamu Mok ...1984 Volume 27 Issue 2 Pages 107-112
Published: February 29, 1984
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSIn order to investigate the dynamics of renin release in diabetes mellitus, the renin activity was measured in streptozotocin (30mg/kg and 60mg/kg)-induced diabetic rats in vivo (furosemide administration test) and in vitro (perfusion study of isolated rat kidney). In the in vitro tests, the kidney was perfused at 4.0ml/min for 20 min, and then the flow rate was decreased to 2.0ml/min for 10 min. The perfusate renin activity was measured by radioimmunoassay, using renin free plasma obtained from bilaterally nephrectomized rabbits as renin substrate. The basal and stimulated renin release from the isolated kidney of streptozotocin-induced diabetic rats were not different from those of control rats. In the in vivo experiments, the plasma renin activity (PRA) was measured before and after furosemide injection. The basal and furosemide-stimulated PRA levels were significantly lower in streptozotocin (60mg/kg)-induced diabetic rats than in controls and streptozotocin (30mg/kg)-induced diabetic rats.
These results suggest that the PRA level is decreased in severe diabetic rats due to secondary effects of diabetes on renin secretion, although the ability of the kidney to secrete renin is maintained.View full abstractDownload PDF (893K) -
Hiroshi Sekimoto, Osamu Katayama, Yoshihide Matsutani, Osafumi Shimada ...1984 Volume 27 Issue 2 Pages 113-119
Published: February 29, 1984
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSHypoglycemia induced by injection of insulin leads to dysfunction of the central nervous system. However, there have been few studies on the changes in ultrastructure of the cerebral vascular system caused by the hypoglycemia. In the present study, we investigated the ultrastructure of the cerebral arterial endothelium using scanning (SEM) and transmission electron microscpy (TEM), in male Wistar rats of normal blood pressure and spontaneously hypertensive rats (SHR) which were treated with insulin (Actrapid, 1.0 unit/100g body weight).
1) The death rate from hypoglycemic convulsions in SHR was 100.0%, which was significantly higher than that of normal rats, 16.7%.
2) SEM observations of the luminal surface of the middle cerebral artery revealed that there were ultrastructural differences in the microvilli and marginal folds of the endothelium between intact normal rats and intact SHR.
3) Injection of insulin caused detachment or disappearance of the endothelium and the occurrence of craters along the marginal folds in both groups. The damage was more prominent in SHR.
4) TEM observations revealed that there were some damaged endothelial cells whose cytoplasmic ultrastructure had been mostly lost in insulin-treated rats. Leakage of red blood cells into the extravascular space was also observed. Fifty-five % of the red blood cells had an unhomogeneous stroma.
These results suggest that insulin-induced hypoglycemia causes ultrastructural damage of the cerebral arterial endothelium, leakage of blood components through the marginal folds and bleeding, and that such damage is more remarkable in SHR.View full abstractDownload PDF (10938K) -
Yasuhiko Kido, Arimasa Hososako, Yoshihiro Nakamura, Mitsuo Ito, Toru ...1984 Volume 27 Issue 2 Pages 121-129
Published: February 29, 1984
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSIn order to clarify the prevalence of diabetic retinopathy and impaired vision cansed by retinopathy, we studied3841consecutive diabetic patients attending 16 diabetes clinics in Fukuoka Prefecture from Dec. 1, 1981 to Jan. 31, 1982.
Diabetic retinopathy was found in29.8% of the patients, and the proliferative type manifested itself in4.6%. Cataract and cataract extracted were noted in16.2and3.0%, respectively.
Retinopathy became more prevalent with increasing duration of diabetes, and50.0% o patients had retinopathy after11to15years of diabetes. In44young dabetics under21years of age, proliferative retinopathy was not found except in one young woman whose duration was16years.
Retinopathy was not present in any of20patients of0to5years duration, but simple retinopathy was present in24% of those (5of21cases) at6to10years duration. Hypertension was more common in cases with simple retinopathy than in cases without retinopathy (24.7vs. 14.5%).
Out of the3841diabetics, impaired vision (visual acuity of20/200or less with best correction) in both eyes and blindness (total visual acuity of8/200or less in both eyes) caused by retinopathy were present in92cases (2.4%) and48cases (1.2%), respectively.
There were153patients (4.0%) with impaired vision in one or both eyes caused by retinopathy. Their mean age, time lapse until the appearance of visual impairment after diagnosis, and untreated period were55.9± 11.5, 10.5 ± 6.0, and 4.2 ± 4.9 (± S.D.) years, respectively.
It could be concluded therefore that in Japan at present, 4to5% of diabetics have diabetic proliferative retinopathy and about1% lose their sight due to retinopathyView full abstractDownload PDF (1203K) -
Hiroyuki Hosojima, Ikuo Yamamoto, Toshikazu Kigoshi, Kenzo Uchida, Shi ...1984 Volume 27 Issue 2 Pages 131-138
Published: February 29, 1984
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSA 67-year-old woman with a 15-year history of diabetes mellitus developed hyperosolar nonketotic diabetic coma and myocardial infarction.Severe metabolic acidosis, however, was observed with marked increases in serum lactate and pyruvate.This represents a rare instance of lactic acidosis complicating hyperosolar nonketotic diabetic coma and myocardial infarction.It appears that the lactic acidosis in the patient may have been induced by multiple factors such as hyperglycemia, infection, dehydration, myocardial infarction, and progression of bleeding probably by DICView full abstractDownload PDF (3840K) -
Moriharu Misaki, Teruo Shima, Kazuhide Adachi, Yasuhiro Sumita, Masats ...1984 Volume 27 Issue 2 Pages 139-141
Published: February 29, 1984
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSTransferrin (Tf) is the chief iron-transport protein in mammalian blood.
Seventy-four diabetics 43 males and 31 females ranging in age from 14 to 79 yr were studied. In all cases, urine protein was negative, and Hb and liver function were normal.Serum fasting blood sugar (FBS), albumin, the integral IRI value after50gOGTT and Tf were measured.The Tf was estimated by laser immunoassay. There was no significant difference between the serum Tf levels of diabetic subjects and normal controls (287±43mg/dl vs.305±37mg/dl, mean±SD) However, the serum Tf levels in subjects with IDDM were significantly lower than those in the normal controls and subjects with NIDDM (249±41mg/dl vs.305±37, 299±36mg/dl;p<0.001).
The serum Tf levels in diabetics were significantly correlated with the serum albumin levels (r=0.366, p<0.002, n=74), FBS (r=-0.338, p<0.02, n=55) and integral IRI values (r=0.608, p<0.002, n=25).View full abstractDownload PDF (1391K) -
Shigeki Sakata1984 Volume 27 Issue 2 Pages 143-146
Published: February 29, 1984
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSRabbit anti-human thyroxine binding globulin (TBG) was precipitated with 50% ammonium sulfate, followed by passage through a DEAE-cellulose column.The immunoglobulin G (IgG) fraction so obtained was covalently attached to Sepharose CL-4B and used as an immunoadsorbent of serum TBG.
After treatment with charcoal to remove endogenous thyroid hormones, 25ul of serum from5 healthy subjects was incubated with 125I-T3 andvarious concentrations of cold T3, 8-anilino-1-naphthalene sulf nic acid (ANS), tolbutamide, chlorpropamide and glibenclamide, followed by immunoadsorption with anti-TBG Sepharose.
The binding of 125I-T3 was inhibited by cold T3 and ANS, whereas sulfonylurea drugs exerted no effect on the interaction between TBG and T3 at concentrations of between 2 and 200mg per dl of serum.
These results, in contrast to the previous report of Hershman et al., suggest that sulfonylurea drugs at serum concentrations which would be expected from their daily therapeutic doses, do not affect the interaction between TBG and T3.View full abstractDownload PDF (456K) -
1984 Volume 27 Issue 2 Pages 147-173
Published: February 29, 1984
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSDownload PDF (4687K)
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