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Volume 38, Issue 5
Displaying 1-12 of 12 articles from this issue
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The Role of Macrophages in the Onset of PVLMasahiko Nakai1995 Volume 38 Issue 5 Pages 333-339
Published: May 30, 1995
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSVascular endothelium is known to play an important role in cell-mediated immune responses. Venular permeability can be detected in vivo by injecting an animal with colloidal pigment, such as Monastral Blue B (MbB), and increased pancreatic vanular leakage (PVL) demonstrated with M bB was observed in spontaneously diabetic BB/W rats. In this experiment we investigated the relationship between PVL and insulitis in BB/W rats, and assessed the physiological charcateristics of this phenomenon to explore the role of PVL in the development of autoimmune diabetes.(1) In young BB/W rats, PVL was observed prior to insulitis. In older rats with insulitis, the intensity of PVL was closely correlated with the severity of the insulitis.(2) PVL was suppressed by pretreatment with superoxide dismutase and catalase, which removed the hydroxyl radicals.(3) Serum levels of TNF α in BB/W rats were marekedly increased by injection of MbB (basal: 0 U/ml, MbB: 28 ± 8 U/ml).(4) PVL was almost blocked of the first day after injection of macrophage-toxic silica, but was gradually restored and recovered entirely 8 days after the injection Long-term administration of silica to young BB/W rats almost completely prevented PVL and the development of spontaneous diabetes. These findings suggest that PVL may participate in the development of the disease and that macrohages may play an important role in the onset of PVL.View full abstractDownload PDF (990K) -
Eiji Kawasaki, Norio Abiru, Mayumi Yano, Miwa Ishibashi, Hidefumi Yama ...1995 Volume 38 Issue 5 Pages 341-346
Published: May 30, 1995
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSWe assayed antibodies to glutamic acid decarboxylase (GAD), a known diagnostic and predictive marker for type I diabetes, in 114 insulin-treated patients initially diagnosed with NIDDM, and examined the clinical characteristics of these antibody-positive subjects. The overall prevalence of GAD antibodies was 16.7%(19/114). When the patients were classified according to postprandial serum C-peptide levels (more or less than 1.0ng/ml) into non insulin deficient group and an insulin-deficient group, the prevalence of GAD antibodies in the insulin deficient group (35.9%; 14/39) was significantly higher than in the non-insulin-deficient group (6.7%; 6/75). ICA was detected in 12 (63.2%) of the 19 GAD antibody-positive patients. Furthermore, the patients with GAD antibodies exhibited clinical features of type I diabetes, characterized by a shorter duration until insulin theraphy, lower body mass index and lower insulin secretion. These results suggest that GAD antibodies are useful marker for detecting type I diabetes in patients intially diagnosed with NIDDM.View full abstractDownload PDF (730K) -
Tetsuya Babazono, Satoshi Teraoka, Masanobu Takeda, Yumiko Sakka, Kaor ...1995 Volume 38 Issue 5 Pages 347-352
Published: May 30, 1995
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSTo determine whether kidney transplantation contributes to improving the mortalityof diabetic patients with end-stage renal disease, we compared survival data of 21 diabetic kidney transplant recipients with those of 247 diabetic patients undergoing dialysis therapy and those of 615 non-diabetic kidney transplant recipients. The overall patient survival after the onset of dialysis was significantly higher in the diabetic transplant group than in the diabetic dialysis group: 94.1% versus 59.8% at 5 years and 78.4% versus 37.7% at 10 years (p =0.011). After adjusting age at the onset of dialysis, sex, and co-morbid conditions using the Cox's proportional hazards model, kidney transplantation had an improving effect on patient survival with a relative risk of 0.336 for transplantation in reference to dialysis. The overall graft and patient survival after transplantation did not differ significantly between the diabetic and non-diabetic recipients at 5 years: 83.5% and 90.5%, in the diabetic group and 74.8% and 89.2% in the non-diabetic group. In conclusion, kidney transplantation is an effective therapeutic modality also in patients with diabetes mellitus concerning to lower mortality than dialysis.View full abstractDownload PDF (1042K) -
Yoshio Nakano, Tokio Sanke, Tadashi Hanabusa, Chikato Oki, Hiroki Jiko ...1995 Volume 38 Issue 5 Pages 353-358
Published: May 30, 1995
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSIslet amyloid polypeptide (IAPP) is belived to be a biologically active peptide co-secreted with insulin by pancreatic B-cells. Many investigators have focused on the relation between this putative peptde and the pathophysiology of NIDDM. In this study, fasting plasma IAPP concentrations and responses to injection of 10 g glucose and 1 mg glucagon (GG test) were measured in NIDDM and borderline glucose intolerance (BDR), and compared with those of C-peptide (CPR) to assess the characteristics of IAPP secretion in NIDDM.
The fasting IAPP/CPR molar ratio was low in NIDDM patients, especially in patientsin the subgroup with a high fasting CPR level and those treated with glibenclamide. This suggests hypo-secretion of IAPP relative to insulin in NIDDM patients whose pancreatic B-cells are chronically stimulated. The GG test revealed that the reserve capacity of pancreatic B-cells to secrete IAPP was reduced more than their reserve capacity to secrete insulin, even in the stage. These results suggest the existence of IAPP hypo-secretion relative to insulin in BDR and NIDDM patients, and this may be related to the development of NIDDM.View full abstractDownload PDF (936K) -
Kazunori Konaka, Hideki Hidaka, Hideto Kojima, Yukio Shigeta1995 Volume 38 Issue 5 Pages 359-366
Published: May 30, 1995
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSThe effects of insulin on cholesterol esters accumulation and its transepithelial secretion (from the upper to the lower medium) in human intestinal cell line CaCo-2, cultured on membrane filters as an in vitro model of the small intestine, were studied during stimulation of the rate limiting enzyme of cholesterol esterification, acyl CoA: cholesterol acyltransferase (ACAT), with 25-OH cholesterol to investigate the mechanism of increased cholesterol absorption efficiency in diabetes mellitus. In the presence of oleic acid (500 itM) in the upper medium, 25-OH cholesterol (10 μg/ml) enhanced [14C] cholesterol esterification in the cells 3 folds (1770±21 vs 561±8 pmol/well/48 hours) and resulted in a fold increase in secretion of esterified [14C] cholesterol (78.9±2.6 vs 39.1±2.1 pmol/well/48 hours). In the absence of oleic acid, howerer, 25-OH cholesterol did not change esterified [14C] cholesterol secretion into the lower medium (26.1±1.5 vs 26.5±0.5 pmol/well/48 hours), although [14C] cholesterol esterification in the cells was increased by 5 fold (301±16 vs 61.3±2.6 pmol/well/48 hours). Insulin (5 μ/m/) added to the lower medium inhibited the secretion of esterified [14C] cholesterol into lower medium both in the presence and absence of oleic acid. These effects were observed when cholesterol esterification in the cells was enhanced by 25 OH cholesterol. Insulin inhibited micellar [14C] cholesterol esterification in the cells and the transepithelial secretion dose-dependently, and the insulin concentration for a half maximal effect was approximately 5-10 ng/ml. These results indicated that the transepithelial cholesterol ester secretory activity of CaCo-2 cells is regulated not only by intracellular ester accumulation but by other mechanisms, including triglyceride formation and/or the assembling of lipoproteins, and suggest that the increased cholesterol absorption efficiency in diabetes is not explained solely by increased ACAT activity, but by increased lipoprotein secretory activity in the gut associated with insulin deficiency.View full abstractDownload PDF (1225K) -
Kiyoshi Kunika, Seiji Suzuki, Kamejiro Yamashita, Mitsuo Itakura1995 Volume 38 Issue 5 Pages 367-374
Published: May 30, 1995
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSTo evaluate themechanism of diabetic albuminuria (DA), an assay method for the negative charge (NC) of albumin (ALB) with variable degrees of glycation based on alcian blue (AB) binding was developed. In the in vitro study, AB billding capacity (ABBC), defined as the decrease in absorbance at 650 nm of the AB solution supernatant, increased linearly with an increasing amount of serum and urinary protein, or purified ALB, but no ABBC was detected with purified γ-globulin. ALB was shown to be a major binding component not only by celluloseacetate electrophoresis of serum and urine sample safter incubation with AB, but by the reciproncal relationliship between ABBC and free ALB concentrations in AB solution supernatants in vitro.ABBC was positively correlated with serum glycated ALB (S-GA) concentration and increased pH, and was negatively correlated with NaCl concentration.In the in vivo study in subjects with micro albuminuria, a reciprocal relationship was found between SGA and urinary glycated ALB (UGA). and between S-GA and urinary ABBC in non diabetic conitrol subjects, but this changed to a positive correlation in patients with diabetes when SGA exceeded 17.6%. In sublects with macro-albuminuria, U-ABBC was low and no correlation between S GA was observed in eiher control subjects or patients with diabetes.
It is concluded that the NC assay based on ionic ABBC is useful as an index of ALB g1ycatlon, and that the mechanism of urinary ALB excretion in the patients with DA, but not in the control subjects with non-diabetic albuminuria, was CB damage.View full abstractDownload PDF (1090K) -
Kaoru Iso1995 Volume 38 Issue 5 Pages 375-382
Published: May 30, 1995
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSTo clarify whether angiotensin-converting enzyme inhibitor (ACEI) prevents the development of nephropathy in streptozotocin (STZ)-induced diabetes in spontaneously hypertensive rats (SHR), changes in creatinine clearance (Ccr) and urinary albumin excretion rate (UAE) were observed for 4 weeks. At the end of the experiment the numbers of anionic sites (AS) on the lamina rara externa of the glomerular basement membrane (GBM) were evaluated in the following five groups:(1) control SHR, (2) ACEI-treated SHR (SHR-ACEI), (3) STZ-induced diabetic SHR (SHR-STZ), ACEI-treated (week 1 to 4) STZ-induced diabetic SHR (SHR-STZ-ACEI), (5) ACEI-treated (week 3 to 4) STZ-induced diabetic SHR (SHR-STZ-late ACEI). Elevation of Cc, -was found to have been suppressed in SHR-STZ-ACEI when compared with SHR-STZ. The increase in UAE in the SHR-STZ was also suppressed in the two ACEI-treated diabetic SHR groups, and the decrease in number of AS in the SHR-STZ was prevented in the two ACEI-treated diabetic SHR groups.
From these results, ACEI appears to prevent the development of nephropathy in STZ-induced diabetic SHR by suppressing the increase in blood pressure and mitigating the increase in permeability of the GBM.View full abstractDownload PDF (3172K) -
Shin-ichi Umezawa, Akira Kanamori, Masako Noguchi, Rika Ohwada, Tatsum ...1995 Volume 38 Issue 5 Pages 383-388
Published: May 30, 1995
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSA 55-year-old female diabetic patient was admitted to Kitasato University Hospital with a diagnosis of diabetic coma. She had a 10-year history of NIDDM and was being treated with insulin (20 U per day). She had discontinued insulin injection for a few days before admission because of appetite loss and vomiting. On admission, physical examination disclosed arterial obstruction in the right leg. Fogarty catheter thrombectomy was performed along with fluid replacement and insulin supplementation, and a large number of thrombi were removed. Despite the patency of the main artery after thrombectomy, peripheral blood circulation could not be achieved. Urokinase thrombolytic therapy was then instituted, but failed to restore peripheral blood circulation in the affected leg. The patient developed disseminated intravascular coagulopathy, and ultimately above-the-knee amputation of the leg saved her life. Both the preoperative angiographic findings and the results of pathohistological examination of the amputated leg showed only minimal arteriosclerotic changes. We concluded that the mechanism of arterial occlusion in this case was based mainly on a hypercoaguable state (hemostatic factor) associated with diabetic coma, and not on endothelial damage due to atherosclerosis and arteriosclerosis (vascular factor).View full abstractDownload PDF (5244K) -
Shinobu Tanabashi, Masahiro Mihara1995 Volume 38 Issue 5 Pages 389-394
Published: May 30, 1995
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSWe encountered a 76-year-old female diabetic patient who developed hypoglycemia induced by miconazole during treatment with gliclazide. She was diagnosed as having diabetes mellitus at the age of 55 years. She had been treated with gliclazide in our department for 5 years. On admission she had proliferative retinopathy and proteinuria. A chest x-ray taken in September 1992 revealed a tumor shadow with air-fluid level in the right upper lung. After being admitted, 400 mg of miconazole was administered intravenously during treatment with 40 mg of gliclazide. Five days later the patient developed hypoglycemia. Her blood glucose levels ranged from 30 mg/d/ to 40 mg/d/ in spite of glucose infusion. Two days after gliclazide was discontinued, fasting blood glucose was 36 mg/d/, and serum IRI and CPR were 13.5 μU/m/ and 4.1 ng/m/, respectively. These findings suggested possibility of insulin hypersercretion. There was no evidence of insulinoma on ultrasound and CT examination of the abdomen. We therefore determined the serum concentrations of gliclazide. The serum gliclazide level during hypoglycemia (36 mg/d/) increased to 4.6 pg/m/ in spite of discontinuation of gliclazide two days earlier, whereas the fasting level of gliclazide on admission was 0.2 pg/mi. These results suggest that the hypoglycemia may have been caused by the higher serum gliclazide concentration resulting from an interaction between miconazole and gliclazide.
Miconazole may interfere with gliclazide metabolism by inhibiting the hepatic cytochrome P450 enzyme system. Imidazole antifungal agents, including miconazole, must be used carefully during treatment with oral hypoglycemic agents.View full abstractDownload PDF (828K) -
Nobuhiko Kuramoto, Ryukou Chou, Chung I Haung, Kazuo Yagui, Osamu Noza ...1995 Volume 38 Issue 5 Pages 395-400
Published: May 30, 1995
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSA 49-year-old woman developed insulin-dependent diabetes mellitus (IDDM) during interferon-α(IFN-α) therapy for chronic myelogenous leukemia (CML). CML was diagnosed in 1985. She had been receiving hydroxyurea and ubenimex since 1985, but in June 1991, her CML became exacerbated and recombinant IFN-α2b (Schering) was started at 6 MU twice weekly. During treatment her white blood cell count was controlled within normal range, but the Philadelphia chromosome persisted. In July, 1993, the patient experienced the sudden onset of thirst, polyuria, polydipsia and general malaise. She was hyperglycemic, had high HbA1c levels and ketonemia with low serum and urinary C-peptide. Islet-cell antibody (ICA) was detected, but islet cell surface antibody (ICSA) was not. HLA-typing yielded: DR4/DR9, DRB10405, 0901, DQA10301 and DQB10401, 0303. The thyroid microsome antibody titer was above normal, and thyroid function test results were just below the normal range. This patient may have had genetic susceptibility to IDDM and developed this disease during IFN-α therapy. Treatment may have elicited a pancreatic autoimmune process, inducing pancreatic, β-cell destrution.View full abstractDownload PDF (789K) -
Matsuo Taniyama, Yoshihiko Suzuki, Shou Enomoto, Yutaka Sato, Eri Sugi ...1995 Volume 38 Issue 5 Pages 401-404
Published: May 30, 1995
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSThe substitution of guanine (G) for adenine (A) at positioln 3243 of mitochondrial DNA, first demonstrated in MELAS patients, has been found in some diabetics, and this mutation seems to be one of genetic factors for diabetes mellitus. Because mutational mitochondria coexist with normal mitochondria (heteroplasmy), conventional PCR-RFLPm methods may not detect a mutation When a majority of the mitochondrial DNA in leukocytes is normal. We tested the efficacy of specific PCR amplification in detecting the 3243G mutation using a primer whonse 3' base was complementary to the mutational base. This mutation-specific PCR amplification method permitted detection of the mutation in 2 patients with MELAS and in a diabetic patient whose mutation was detected by the PCR-RFLP method in biopsied muscle but not in peripheral leukocytes, and in two other diabetic patients.Specific PCR amplification for detection of the 3243G mutation is a simple and senisitive method and is useful inevaluating this mutation in diabetes mellituls.View full abstractDownload PDF (541K) -
Kosaku Nitta, Wako Yumura, Hiroshi Nihei1995 Volume 38 Issue 5 Pages 405-408
Published: May 30, 1995
Released on J-STAGE: March 02, 2011
JOURNAL FREE ACCESSIn order to assess glomerular endothelial permeability, we established an in vitro model using an immortalized bovine glomerular endothelial cell line. We examined the effect of high glucose concentration on albumin permeability across glomerular endothelial cell monolayers. Thirty millimolar D-glucose doubled albumin permeability (12.1±1.3%) compared with 10mM D-glucose (6.4±0.8%), but the albumin permeability of endothelial cells exposed to 10mM glucose+20mM mannitol was 6.8+0.5%. In addition, H-7 (25μM), a protein kinase C (PKC) inhibitor, suppressed the increased albumin permeability induced by 30mM glucose (7.8±0.9%). Lactate dehydrogenase release by endothelial cells incubated with 30mM glucose, on the other hand, was no different than when incubated with 10mM glucose, indicating that cytolysis was not associated with these events. These findings suggest that PKC activation is an important signal transduction pathway by which high glucose concentration increases glomerular endothelial albumin permeability.View full abstractDownload PDF (417K)
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