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Volume 32, Issue 2
Displaying 1-8 of 8 articles from this issue
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Riku Nomiyama, Kiyohide Nunoi, Yasuo Watanabe, Masanori Wakisaka, Yuki ...1989 Volume 32 Issue 2 Pages 85-89
Published: February 28, 1989
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSUrinary albumin excretion was determined in 54 IDDM children without macroproteinuria (Albustix) and in 18 age-and sex-matched nondiabetic subjects. The diabetic group averaged 12.5 years of age and had had diabetes for an average 4.8 years. Urinary albumin was measured by the immunoturbidity method using a postprandial urine sample and expressed by the amount per gram of creatinine (urinary albumin index: UAI, mg/g·Cr). A cross-section of 54 patients was studied, and 22 of them were studied again 3 years later. The results were as follows:
1) Microalbuminuria, i.e., albumin at a level of more than 24 mg/g·Cr (mean+2 SD value of normal), was detected in 20% of diabetics.
2) UAI did not correlate with recent glycemic control at different periods.
3) Although only 1 out of 22 patients showed persistent microalbuminuria and the UAI value fluctuated in some cases, the group with initially high UAI (≥17 mg/g·Cr, mean+1 SD value of normal) tended to show high UAI 3 years later.
4) The higher the index of HbA1c (%)×duration of diabetes (months), the more frequent the patients who showed high UAI at initial or follow-up examination.
These date suggest that some disorders develop in the kideny after a short duration of IDDM and that long-term rather than short-term hyperglycemia may contribute to the development of transient microalbuminuria.View full abstractDownload PDF (803K) -
Masako Waki, Hideki Koh, Seiki Nambu1989 Volume 32 Issue 2 Pages 91-96
Published: February 28, 1989
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSTo clarify the clinical significance of the serum 3, 5, 3'-triiodothyronine (T3) level in NIDDM on diets containing 200-300 g carbohydrate, the relationship between the T3 level and other conventional parameters was studied in 79 non-insulin-dependent diabetic inpatients. Furthermore, in 65 of these patients, the relationship between T3 leval and the efficacy of diet therapy was analyzed retrospectively. Results were as follows:
1) In the 79 patients, the T3 level was significantly correlated with the duration of diabetes (r=-0.28), fasting plasma glucose (r=-0.37), HbA1c (r=-0.28), body mass index (r=0.48), NEFA (r=0.40), T4 (r=0.32) and 24-hour urinary C-peptide excretion (r=0.35).
2) The 65 patients were divided into two groups according to the results of diet therapy: Group D (n=29), whose glycemic control was achieved by diet therapy alone, and Group D+M (n=36), whose glycemic control required medication. In Group D, T3 levels were more than 110ng/dl in 90% of the patients, but in Group D+M, T3 levels were less than 110 ng/dl in 64% of the patients. Accordingly, the distribution of T3 levels between the two groups was statistically different (χ2= 17.0, p<0.001).
In conclusion, the serum T3 level reflects overall metabolic derangement in NIDDM, and its measurement enables us to predict the efficacy of diet therapy.View full abstractDownload PDF (962K) -
Yoshihiko Nishio1989 Volume 32 Issue 2 Pages 97-103
Published: February 28, 1989
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSThe number of cell-surface β-adrenergic receptors on cardiomyocytes isolated from diabetic rats, as determined by the hydrophilic ligand [3H] CGP-12177, decreased significantly to 59% of that in control rats (p<0.01), while the number of total cell β-adrenergic receptors, as determined by the hydrophobic ligand [125I] ICYP, did not differ between the two groups. Adenylate cyclase activity in cardiac plasma membrane isolated from diabetic rats also decreased significantly to 48% of the control level (p<0.05). Forty-eight hour in vivo insulin treatment improved the decrease in the number of cell-surface β-adrenergic receptors without causing any changes in serum T3 level or urinary catecholamine excretion rate. Insulin, high levels of glucose, and 3-hydroxybutyrate levels did not affect [3H] CGP-12177 binding to cardiomyocytes. Furthermore, diabetic cardiomyocytes showed significant (p<0.05) impairment in their recovery from agonist-induced down-regulation as compared with the control level.
These results indicate that the decrease in the number of β-adrenergic receptors in cardiac plasma membrane, which is associated with abnormalities in the receptor distribution, played an important role in the cardiac unresponsiveness to a β-adrenergic agonist in diabetic rats. The decrease in the number of receptors in plasma membrane is closely associated with the diabetic state and is reversed by short-term insulin treatment.View full abstractDownload PDF (1272K) -
Tetsurou Arimura1989 Volume 32 Issue 2 Pages 105-111
Published: February 28, 1989
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSThe impairment of mesangial cell function was recently found in renal glomeruli isolated from streptozocin-induced diabetic rats. Since mesangial cells possess the polyol pathway, the accumulation of sorbitol in the diabetic state has been suggested to be causally related to mesangial cell dysfunction. However, the precise mechanism of mesangial cell dysfunction has not been clarified. In order to further elucidate the metabolic abnormalities of these cells induced by high concentrations of glucose, myo-inositol metabolism was evaluated in cultured rat mesangial cells.
By exposing the cells to a high concentration of glucose (55mM), the intracellular myo-inositol content was significantly decreased from 11.0±1.0 to 2.8±0.5 nmol/mg protein, and the sorbitol content was increased 12-fold. These changes were revealed in a dose-dependent manner, and reversed by aldose reductase inhibitor. In order to examine the mechanism of myo-inositol depletion, the uptake of myo-inositol by mesangial cells was studied. Most myo-inositol uptake was Na-dependent and saturable. Glucose inhibited myo-inositol uptake in a dose-dependent manner and kinetic analysis using Lineweaver-Burk and Dixon plots revealed that the inhibition was competitive. The addition of aldose reductase inhibitor was not able to prevent the inhibition of myo-inositol uptake. In conclusion, under the excess of ambient glucose, intracellular myo-inositol content was decreased partly via the reduction of myo-inositol uptake produced by glucose. These metabolic derangements might be responsible for the impairment of mesangial cell function.View full abstractDownload PDF (1342K) -
Tsyoshi Takamatsu, Tsuguhiko Nakai, Toshitaka Tamai, Hirotaka Takai, S ...1989 Volume 32 Issue 2 Pages 113-119
Published: February 28, 1989
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSThe patient was a 66-year-old male with noninsulin-dependent diabetes mellitus complicated by adult respiratory distress syndrome (ARDS). He had received no therapy since he was first diagnosed as having diabetes mellitus at 54 years of age. In November 1986, he developed gangrene on the bilateral toes and was treated with insulin and intravenous prostaglandin E, infusion. In January 1987, bypass graft operation was performed on the right femoral artery. Fever, dyspnea and edema appeared 10 days after the operation, followed by pulmonary edema on chest X-P and hypoxemia (PaO2 34.3mmHg). These were not improved by conventional therapy with oxygen inhalation and diuretics. Therefore, the patient was transferred to our university hospital and treated by mechanical ventilation with high oxygen content and the use of positive end expiratory pressure and diuretics. Pulmonary edema and hypoxemia recovered in 2 weeks. These clinical features were compatible with ARDS. It is postulated that low plasma osmotic pressure, suggested by a low hematocrit value and hypoalbuminemia, which may be caused by high volume crystalloid infusion after surgery, respiratory tract infection and an increase in the permeability of pulmonary capillary membranes possibly related to the diabetic state, might have precipitated the acute respiratory complications.View full abstractDownload PDF (2563K) -
Mitsuaki Takeda, Ichiro Michisita, Nobuo Kamon, Yohei Tofuku, Junji Ko ...1989 Volume 32 Issue 2 Pages 121-126
Published: February 28, 1989
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSWe report a case of insulin-dependent diabetes mellitus (IDDM) associated with diabetic microangiopathic hemolytic anemia (MHA).
The patient was a 23-year-old woman who had a history of diabetes for 14 years, with significant diabetic triopathy (diabetic retinopathy of Scott II a, diabetic glomerulosclerosis and peripheral neuropathy of upper and lower extremities). She had required daily injections of insulin since the age of 9 years and started intensive therapy with continuous subcutaneous insulin injection of 21 years of age. She was admitted to our hospital because of generalized edema, hypertension and severe anemia, at the age of 23 years. Laboratory data showed increased LDH (857 IU/l), renal failure (Cr 1.8mg/dl, BUN 36mg/dl), anemia (hemoglobin concentration 6.5g/dl, hematocrit 19.2%) and decreased haptoglobin level. Marked fragmentation of red cells was seen in peripheral blood smears. There were no enzyme deficiencies leading to hemolytic anemia. Moderate bone marrow hyperplasia was found. The 51Cr disappearance half-time was decreased to 14 days. In spite of poor control of blood glucose levels, Hb A1 and Hb A1c concentrations were low. These data indicated severe microangiopathic hemolytic anemia. After continuous ambulatory peritoneal dialysis therapy, her blood pressure was normalized and anemia improved. Microangiopathic hemolytic anemia may be produced by diabetic microangiopathy and hypertensive vascular injury.View full abstractDownload PDF (2163K) -
Yuri Ono, Masahiko Katoh, Mamoru Kudoh, Shoichi Nakagawa, Aizan Hirai, ...1989 Volume 32 Issue 2 Pages 127-130
Published: February 28, 1989
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSMeasured levels of plasma thromboxane B2 (TXB2) do not reflect endogenous thromboxane (TX) production precisely, because mechanical stimulation of platelets during blood sampling may cause TXB2 production. il-Dehydro TXB2 (11-DTX) which is one of the major metabolites of TXB2 and is not converted from TXB2 by blood cells or plasma, is considered suitable as a target for measurement of TX production in vivo. We measured, by radioimmunoassay, plasma TXB2, 11-DTX and the ability of platelets to produce TXB2 during spontaneous clotting (TX production) in 46 diabetics and 31 normal controls.
Plasma TXB2 concentration and plasma 11-DTX concentration were higher in diabetics than in normal controls, but TX production did not differ between diabetics and normal controls. The plasma TXB2/11-DTX ratio had a tendency to be higher in diabetics than in normal controls. These results suggest that in diabetics, the high concentrations of plasma TXB2 and 11-DTX are caused by high concentrations of circulating TXA2 in vivo; and the high plasma TXB2/11-DTX ratio in diabetics may also indicate a tendency for increased synthesis of TXB2 during blood sampling in diabetics.View full abstractDownload PDF (545K) -
1989 Volume 32 Issue 2 Pages 131-153
Published: February 28, 1989
Released on J-STAGE: August 10, 2011
JOURNAL FREE ACCESSDownload PDF (6225K)
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