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Volume 30, Issue 5
Displaying 1-10 of 10 articles from this issue
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Application in the Evaluation of Minimal Residual B-cell Function in IDDMMasahiro Fukuda, Akira Tanaka, Yasuhiro Tahara, Hiroshi Ikegami, Yoshi ...1987 Volume 30 Issue 5 Pages 395-401
Published: May 30, 1987
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSWe have developed a highly sensitive C-peptide (CPR) assay and investigated whether any residual B-cell function is present in IDDM patients whose fasting CPR and/or CPR responses to iv glucagon (1 mg) could not be demonstrated by a conventional assay.
Highly sensitive assay-Three ml of plasma sample was extracted with 6ml of 96 %(V/V) ethanol and the extract was evaporated to dryness. The residue was dissolved in 0.3 ml of phosphate buffer and 0.5 ml of trichlorotrifluoroethane was added as a lipid solvent. The aqueous phase was separated by centrifugation and used for radioimmunoassay. The detection limit of this assay was 0.03 ng/ml and the intra-and interassay coefficients of variation were 5.4 and 9.4 %, respectively.
Using this method, significant CPR responses to iv glucagon (Δ CPR 0.19±0.16 ng/ml, mean±SD) were demonstrated in 12 of 21 IDDM patients. The other 9 showed no CPR responses (Δ CPR 0.01±0.01 ng/ml). Hemoglobin A1c and the standard deviation of 10 measurements of fasting plasma glucose (SDFPG) were significantly higher (p<0.05 and p<0.01, respectively) in the latter group. A significant inverse correlation was also found between incremental CPR areas after iv glucagon and SDFPG (r=-0.84, p<0.001).
Our sensitive method for CPR assay is very useful for evaluating residual B-cell function in IDDM patients whose plasma CPR levels are below detection limit by the conventional method. It is suggested that the presence of minimal residual B-cell function plays an important role in metabolic stability in IDDM.View full abstractDownload PDF (1184K) -
Hideo Fukasawa, Nigishi Hotta, Hironobu Kakuta, Masao Kimura, Naoki Ko ...1987 Volume 30 Issue 5 Pages 403-409
Published: May 30, 1987
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSRecently a relationship was found between increased sorbitol concentration and decreased myoinositol in the peripheral nerves of diabetic rats. However, as yet there is no definitive evidence indicating whether erythrocytes are a suitable indicator for monitoring myo-inositol concentration in other tissues.
Therefore, the effects the concentrations of insulin, aldose reductase inhibitor, elevated medium glucose and other metabolites on 2-[3H] myo-inositol uptake were studied in metabolically-defined cultures of erythrocytes from humans, rabbits and rats.
At all concentrations of myo-inositol in the medium (1-5000 μM), 2-[3H] myo-inositol uptake was highest in the rabbit and lowest in the rat. The myo-inositol permeability was increased dosedependently. In human erythrocytes, the myo-inositol uptake was inhibited by increased concentrations of glucose (5-20 mM), fructose (20 mM) and ouabain (2-10 mM). This inhibition was stronger with glucose than with ouabain. However, insulin (200 μU/ml) and aldose reductase inhibitor (ONO-2235, 100 μM) failed to increase the myo-inositol uptake reduced by either 10 mM glucose or 2 mM ouabain. Ouabain at 10 mM inhibited myo-inositol uptake in all species but it was not inhibited by 20 mM glucose in rabbit erythrocytes.
Apparently, the determination of myo-inositol concentration in erythrocytes may not be a suitable indicator for monitoring the state of diabetic complications or for evaluating the possible effect of aldose reductase inhibitor on myo-inositol concentration in other tissues concerned with diabetic complications.View full abstractDownload PDF (1183K) -
Yoshihiko Nishio, Atsunori Kashiwagi, Masahiko Terada, Yukio Hatanaka, ...1987 Volume 30 Issue 5 Pages 411-417
Published: May 30, 1987
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSIn order to clarify the preclinical abnormalities of the cardiac function in subjects with diabetes mellitus without heart failure, we studied the cardiovascular responses to continuous iv infusion of epinephrine.
Subjects: Fourteen diabetic and 6 non-diabetic non-obese individuals (ages 38-60) without any cardiovascular abnormalities such as heart failure, hypertension and electrocardiographic abnormalities were investigated.
Method: Epineprhine was administered by continuous iv infusion at the rate of 1.5 and 3.0 μg/h/kg for 20 min. The cardiovascular response to epinephrine infusion was assessed by using the M-mode echocardiography and continuous blood pressure and pulse rate monitoring system. Increase in the ejection fraction (EF) following the epinephrine infusion above the basal EF was assessed from the echocardiogram by using Teichholtz's equation. The following results were obtained.
Plasma epinephrine levels in the diabetic and non-diabetic subjects were similar. There was no significant difference in basal EF between diabetic and non-diabetic subjects.ΔEF was significantly negatively correlated with the duration of diabetes (r=-0.70, p<0.005), but not with age of the diabetic subjects (r=-0.05, NS).ΔEF in diabetic subjects with a complication was less than that in non-diabetics (p<0.005). In particular ΔEF in diabetics with autonomic neuropathy was further blunted, even though the tachycardic response to the epinephrine infusion in those subjects was significantly accentuated. There was a significant negative correlation (r=-0.86, p<0.005) between ΔEF and the HbA1 levels in diabetic subjects without severe complications.
These results indicate that the response of cardiac function to epinephrine infusion in diabetic subjects without any clinical cardiovascular abnormalities is defective. This defective cardiac response is correlated with either the duration of diabetes, severity of the diabetic complication or glycemic control.View full abstractDownload PDF (1029K) -
Hideto Kojima1987 Volume 30 Issue 5 Pages 419-427
Published: May 30, 1987
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSHormonal regulation and the roles of 3 protein kinases in fatty acid oxidation and ketogenesis have been studied in isolated rat hepatocytes. Glucagon and catecholamines respectively stimulated [U-14C] palmitate oxidation to CO2 by 60% and 25% and to ketone body by 58% and 25% within 1 hour. As forskolin and dibutyl cyclic AMP (d-cAMP) also enhanced hepatic ketogenesis, glucagon-stimulated ketogenesis is thought to be mediated through cAMP-dependent protein kinase (Akinase). Catecholamine-stimulated ketogenesis has been suppressed by prazosin or N-(6-aminohexyl)-5-chloro-1-naphthalene sulfonamide (W-7), but not by yohimbine. This indicates that the catcholamine-stimulated ketogenesis may be mediated through α1-receptor and Ca++-calmodulin-dependent protein kinase. Vasopressin, phorbol 12-tetradecanoate 13-acetate (TPA), or 1-oleoyl-2-acetylgiycerol (diacylglycerol) prevented glucagon-or epinephrine-stimulated ketogenesis, indicating that c-kinase may be mediated in this mechanism. Insulin, GH, T3, or dexamethasone alone had no significant effect on hepatic ketogenesis within 1 hour. When hepatocytes were treated with glucagon or epinephrine, carnitine palmitoyltransferase (CPT), a key regulatory enzyme of palmitate oxidation, was activated. This hormone-induced activation of CPT was not observed in the presence of TPA. These observations suggest that c-kinase inhibits glucagon-or catecholamine-stimulated palmitate oxidation to ketone bodies, and this inhibition may possibly be mediated through a covalent modification of CPT.View full abstractDownload PDF (1342K) -
With Reference to the Relationship between Microalbuminuria and Diabetic Renal LesionShigeki Inomata, Yoshiyuki Oosawa, Masuo Itoh, Masanori Inoue, Osamu M ...1987 Volume 30 Issue 5 Pages 429-435
Published: May 30, 1987
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSIn order to evaluate the renal lesion and the clinical picture in diabetics with microalbuminuria the urinary albumin excretion rate (AER) was assessed and renal biopsy was performed in nonproteinuric (Albustix-negative) diabetics. The following results were obtained.
The resting AER was 6.6±3.8 (mean±SD)μg/min and 21.0±24.8μg/min in 20 healthy controls and 59 non-proteinuric diabetics, respectively. In diabetics, normal (<15 μg/min) and elevated (≥15 μg/min) AER was found in 40 cases (Group A) and 19 cases (Group B) respectively. Group B had longer duration of diabetes, higher systolic blood pressure and a higher incidence of retinopathy than group A.
AER after exercise using an Ergometer was measured in 14 healthy controls and 19 diabetics of group A. No significant differences were found as far as duration of diabetes, HbA1, GFR, max. systolic blood pressure and incidence of retinopathy were concerned. The kidney was similarly damaged in 10 subjects with normal AER and 9 with AER elevated by exercise.
Renal biopsy was performed in 13 subjects in group A, 7 in group B and 5 with persistent proteinuria (group C). The glomerular diffuse lesion (Gellman's classification) was grade O, I or II in group A; II or III in B, and III or IV in C. The glomerular nodular lesion was grade O in A, O or I in B, and I or II in C. Arteriolar hyalinosis (Takazakura's classification) was graded as O or I in A, II or III in B, and III in C.
From these results, it was concluded that 1) diabetics with microalbuminuria had an advanced renal lesion which had the possibility of progress easily into persistent proteinuria and 2) determination of AER induced by exercise is not an adequate method to discriminate the more lerb renal lesion than that in diabetics with microalbuminuria.View full abstractDownload PDF (1269K) -
Fumiyo Hashimoto, Mitsuyo Sato, Chizuko Ohboshi, Meisei Hirota, Ichiyo ...1987 Volume 30 Issue 5 Pages 437-444
Published: May 30, 1987
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSA radioimmunoassay for glycosylated protein (GP) was developed by using an antibody to recuced glycosylated low density lipoprotein which was capable of identifying glucitol lysine epitopes on all reduced GPs studied, including human and bovine albumin. Pretreatment to eliminate free glucose and labile GP from a sample is necessary before measurement of GP in the plasma sample. The mean serum GP value of patients with IDDM (n=32) was 6.06±1.89 n mole of reduced glycosylated lysine equiv. per mg of protein, which was significantly higher than that of normal controls (n=50), 0.824±0.209 n mole of reduced glycosylated lysine euquiv. per mg of protein. The serum GP value in the patients was significantly correlated with their HbA1c level (r=-0.56, p<0.005). The method seems to be promising for further clinical application.View full abstractDownload PDF (1308K) -
Katsunori Nao, Yoshikazu Goriya, Masaru Katsura, Kazuo Hashikawa, Sato ...1987 Volume 30 Issue 5 Pages 445-451
Published: May 30, 1987
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSA 56-year-old male was admitted because of a lacunar stroke and unstable diabetes mellitus requiring 52 units of insulin a day. Abnormal increases in blood glucose occurred during postabsorptive states, namely, in the daytime and late in the evening during the daily glycemic regulations with artificial endocrine pancreas. This was accompanied by concomitant elevations of blood pressure and plasma catecholamine levels. Then a left adrenal tumor, 3 cm in diameter, was found by ultrasonography, abdominal CT scanning and by strikingly high catecholamine concentrations (epinephrine 440 ng/ml, norepinephrine 316 ng/ml) found by selective venous cannulation.
During the operation, rapid changes in glycemia related to the resection of the tumor were safely managed by the use of artificial endocrine pancreas. The patient became insulinindependent after the operation, and well controlled by diet therapy only.
Since the glucagon secretion in response to arginine infusion was normalized after the operation, it is suggested that catecholamine also inhibits pancreatic A-cell function.
Thus, the effectiveness of artificial endocrine pancreas in the diagnosis and the treatment of pheochromocytoma was proven in this case.View full abstractDownload PDF (1151K) -
Kentaro Yamada, Toshiaki Hanafusa, Hiroko Kurihara(Fujino), Yoshitake ...1987 Volume 30 Issue 5 Pages 453-455
Published: May 30, 1987
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSPancreatic tssue was obtained under peritoneoscopy from a 33-year-old man with recently occurring Type I (insulin-dependent) diabetes. He had ICA, CF-ICA and ICSA, and increased DRpositive activated T-lymphocytes. Islets were atrophic and insulin-containing cells were reduced in number, although lymphocytic infiltration was not observed. Most of the islets were positive for DR antigens; DR molecules were detected preferentially on insulin-containing cells. In addition to endocrine cells, pronounced expression of DR antigens was observed on the hypertrophic edothelium of capillaries in and around islets. The expression of DR antigens may be involved in the development of autoimmune reactions to islet cells. Augmented HLA-DR antigens on endothelial cells suggests a possible role of capillary alterations in islet cell damage in Type I diabetes.View full abstractDownload PDF (2842K) -
Masaki Takahashi, Shoji Kawazu, Kiyohiko Negishi, Masao Suzuki, Toshir ...1987 Volume 30 Issue 5 Pages 457-459
Published: May 30, 1987
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSWe determined serum laminin P1 concentrations in normal subjects and diabetic patients in relation to nephropathy, in which glomerular basement membranes are known to be accumulated and thickened. RIA-Laminin P1 Kit (Hoechst Co.) was used for the determination of Laminin P1, a component of lamina lucida of basement membranes.
Serum laminin P1 concentrations in patients with nephropathy, as diagnosed by persistent proteinuria, were significantly higher than those in normals or patients without nephropathy. Moreover, significant relationships were found between serum laminin P1 and daily urinary protein.
Thus, serum laminin P1 can be used as an indicator to signify the progression of diabetic nephropathy or microangiopathy.View full abstractDownload PDF (418K) -
1987 Volume 30 Issue 5 Pages 461-486
Published: May 30, 1987
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSDownload PDF (5375K)
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