Glucosylated plasma protein is one of the glucosylated forms of protein. Recently, Day, Guthrow and McFarland reported that glucosylated albumin and plasma protein could be measured by a method using thiobarbituric acid (TBA), and a significant correlation was observed between hemoglobin Aic (HbAIC) and glucosylated plasma protein. In the present study, it was found that the method for measuring glucosylated plasma protein should be modified in order to exclude glucose from the plasma, since glucose itself is nonenzymatically converted to hydroxymethylfurfural (HMF) which reacts with TBA in the process of measurement of glucosylated plasma protein
The newly modified method for measuring glucosylated plasma protein is briefly as follows. One ml of plasma is dialzed for 24 hours at 4°C with cellulose tubing (Visking Company). Then, 0.1 ml of the dialyzed plasma which contains no glucose is mixed with 0.9 ml of distilled water and 0.5ml of 1 M oxalic acid. The mixture is hydrolyzed at 98°C for 270 min and deproteinized with 40% trichloroacetic acid. 0.5 ml of 2 N HCl and 0.05 M TBA is added to 0.5ml of the supernatant, and the mixture is incubated at 40°C for 30 min. The absorbance is determined at 443 nm with a spectrophotometer. The value of the glucosylated plasma protein is expressed as nmol HMF/mg protein. The concentration of protein is measured by the method utilizing the principle of proteindye binding (Bradford).
The glucosylated plasma protein after exclusion of glucose from the plasma of 5 diabetic patients was 1.36 ± 0.04 (M ± SD) nmol HMF/mg protein, which was less than the 1.55± 0.13 nmol HMF/mg protein in the plasma without glucose exclusion. It was confirmed that the HMF levels converted from 5.5 mM and 13.75 mM of glucose are 0.52 and 0.62 mmol/l, respectively. The concentrations of glucosylated plasma protein in 60 diabetic patients and 15 healthy subjects were 1.43 ± 0.15 and 1.09 ± 0.11 nmol HMF/mg protein, respectively. There was a significant correlation between the glucosylated plasma protein and HbAIC, The newly modified method for measuring glucosylated plasma protein is clearly useful for the assessment of metabolic abnormality in diabetic patients.

View full abstract

Islet cell antibodies (ICA) or islet cell surface antibodies (ICsA) are present in many patients with insulin-dependent diabetes (IDDM). Using cell suspensions of live islet cells, it was found that IDDM patients may have circulating ICsA. We examined whether an association exists between residual beta-cell function and circulating ICsA in diabetic patients. The study represented a cross-sectional investigation of 19% of the diabetic patients visiting our clinic. In the totalgroup of 152 patients, there was no correlation between ICsA and the age at onset or the duration of the disease. The glucose intolerance was greater in IDDM patients with circulating ICsA. The results of the present study thus suggest that circulating ICsA might alter the beta-cell function during the varying stages of diabetes.

View full abstract

Using purified dietary fibers, various authors have reported that their intake is effective in adult diseases such as hyperlipidemia, ischemic heart disease and diabetes mellitus. However, it is difficult to take a large amount of dietary fiber for a long time. It is desirable therefore to ingest dietary fiber as food, and it is important to teach patients to follow a high fiber diet as a habit.
In the present study, the content of dietary fiber of foodstuffs in the exchange table of foods for diabetes mellitus was measured as neutral detergent fiber and calcium pectate, in order to develop a guide for calculating the amount of ingested dietary fiber. The amount of dietary fiber was several times greater than that of crude fiber in the various foodstuffs. Since no trend was observed in the ratios of the two fiber contents, it may be difficult to extrapolate the amount of dietary fiber from that of crude fiber. The table of dietary fiber can be employed as a guide of calculating the amount of fiber ingested.
In a clinical study, after a control period, 14 diabetic subjects with good control were followed for 20-day periods on a 50% fiber rich and isocalory menu, consisting of usual rice or bread and fiber rich dishes. The mean postprandial blood glucose in the daily profile and the urinary sugar were reduced from 193 ± 11 mg/dl (mean ± SEM) to 174 ± 10 mg/dl and from 3.3 ± 1.0 g/day to 1.8 ± 0.6 g/day, respectively. Further investigations involving long-term administration of an increased amount of dietary fiber are required to obtain definite conclusions. However, it is suggested that addition of even a small amount of dietary fiber can be effective in diabetic dietary treatment.

View full abstract

The plasma SFMC concentrations in normal subjects, diabetics without retinopathy, and diabetics without proteinuria were 4.9 ± 1.5, 7.2 ± 4.8, and 6.6 ± 3.8 mg/dl, respectively.
There were no significant differences among these values, In the group with a high blood sugar level of more than 201 mg/dl including many cases of progressive proliferative retinopathy, the SFMC concentration was positively correlated with the blood sugar concentration (r = + 0.59) and also with the fibrinogen concentration (r= +0.71), but it was not related to the antithrombin-III, total cholesterol and triglyceride concentrations. The SFMC levels in diabetics with accompanying proteinuria of under or over 30 mg/dl were both significantly high, at 12.9±10. 1 and 15.2 ± 8.6 mg/dl, respectively.
The SFMC levels in diabetics with retinopathies of Scott IIIa + b and Scott IV-Va were also increased to 14. 3 ± 7.5 and 21.8± 11.9 mg/dl, respectively, but were significantly high only in the group with accompanying proteinuria. The SFMC concentration and the conduction velocity of the aorta or the elastic rate of the carotid were not interrelated. These findings suggest that thrombin generation at some vascular lesions in such patients was indicated by the plasma SFMC production and appeared to accelerate the complication of vascular disorders.

View full abstract

Plasma amino acid levels were analyzed in 4 cases of hyperosmolar nonketotic coma, 6 cases of diabetic ketoacidosis, one case of lactic acidosis before and after corrective therapy, and 7 normal controls. The results obtained were as follows.
(1) In hyperosmolar nonketotic coma, the total amino acids were relatively low, and the amounts of arginine, taurine and serine were decreased both as the concentration and as the molar ratio. The concentration of ornithine was decreased. On the other hand, phenylalanine was increased both as the concentration and the molar ratio, and glutamic acid as the concentration also.
(2) In diabetic ketoacidosis, leucine, isoleucine, glutamic acid, a-aminobutyric acid and valine were increased both as the concentration and as the molar ratio. Histidine, proline, and glycine + citrulline were increased only as the concentration. The level of taurine was lower both as the concentration and as the molar ratio, and that of serine as the molar ratio also.
(3) In the one case of lactic acidosis associated with phenformin administration, tremendous increases in alanine, a-aminobutyric acid and proline were found together with increases in lysine, histidine, threonine, serine, asparagine, glutamine, glycine +citrulline, valine, methionine, isoleucine, leucine, phenylalanine and tyrosine. The concentrations of arginine, aspartic acid, glutamic acid and taurine did not show much change.
The above results appear to indicate differences in the biochemical background to each diabetic coma.

View full abstract

A 73-year-old male case of spontaneous hypoglycemia with auto-antibodies to insulin receptors is reported.
The patient had been well until October, 1977, when he suffered from attacks of perspiration for the first time. Thereafter, similar attacks of perspiration occurred frequently, although there were no episodes of palpitations, fatigue, tremors or nausea during the attacks.
On January 14, 1978, he left dull epigastralgia and anorexia followed for 4 days. On January 19, 1978, he awoke at 5: 00 a.m. with severe perspiration, and thereafter lost consciousness. He was admitted to hospital by ambulance. His blood glucose level was 27 mg/100 ml, and he became alert as soon as he received a glucose injection. That afternoon, attacks of hypoglycemia and unconsciousness occurred once more and hypoglycemia was proved at that time. He began to take meals 5 times a day, and the attacks of hypoglycemia then disappeared.
On March 7, 1978, he was admitted to our hospital in order to examine the cause of his spontaneous hypoglycemia. The patient was remarkably obese (+31%). An oral 100-g glucose tolerance test (o-GTT) revealed supranormal increments of blood glucose levels and serum immunoreactive insulin (IRI) levels. His fasting blood glucose (FBG) and fasting serum IRI levels on the second hospital day were 47 mg/100 ml and 50 μU/ml, respectively. The ratio of IRI to FBG was thus 1.06 (normal, less than 0.5), so that insulinoma was suspected to be the cause of the spontaneous hypoglycemia. However, the tolbutamide test, arginine test, l-leucine test, insulin tolerance test, a scintigram of the pancreas, echogram of the pancreas, computed tomography of the pancreas and selective angiography of the celiac artery, failed to reveal any evidence of insulinoma.
Spontaneous hypoglycemia, glucose intolerance and hyperinsulinemia were also reported in the insulin autoimmune syndrome described by Y. HIRATA in 1970. However, anti-insulin antibodies were not detected in the present patient's serum.
The serum of the patient significantly inhibited the binding of 1251-insulin to membrane pellets of human placenta (60.6%; normal range, 100.8±4.4%). The substances exhibiting the inhibitory effects on the 125I-insulin binding were found to be based mainly in the protein fractions. The existence of anti-insulin receptor antibodies was therefore strongly suspected, and the patient was considered to belong to the type B syndrome of insulin resistance reported by C.R. KAHN in 1976. The abnormal levels of FBG and fasting IRI, abnormal glucose and IRI response to o-GTT and symptoms of hypoglycemia spontaneously improved. Simultaneously, the inhibitory effect of the patient's serum on 125I-insulin binding disappeared. It is suggested that anti-insulin receptor antibodiesmay have played some role in the occurrence of the hypoglycemia in this case. It has been reported that some patients with type B syndrome of insulin resistance may also have acanthosis nigricans or Sjogren syndrome. However, our patient did not display such symptoms, and his onlymajor clinical symptom was spontaneous hypoglycemia.

View full abstract

This report concerns a 30-year-old female who had a baby with Taussig-Bing syndrome. Her diabetes had first appeared at the age of 19 years. Due to genital itching, she then fell into a diabetic coma at the time of admission to a gynecological hospital. An insulin injection was immediately administered upon admission along with fluid treatment, and her condition promptly improved.
Subsequently, however, her diabetic control was poorly maintained. She married at the age of 23 years and became pregnant for the first time one year later. She gave birth to a premature infant and the baby died within a few hours after birt
She became pregnant a second time at the age of 29 years and in the 19th week of this pregnancy, she entered a diabetic precoma and was transferred to our diabetes center. On admission, her blood glucose was high, her blood gas analysis indicated compensated metabolic acidosis, and her ocular fundus was Scott Ia. After frequent injections of insulin, her blood glucose was brought under control and this control was maintained until delivery of the infant. However, her diabetic retinopathy worsened from Scott Ia to IIIb and the infant was delivered by cesarean section at 38 weeks and 4 days. The female infant weighed 3, 375 g.
During physical examination of the baby, a heart murmur, which became increasingly loud, was detected and a radiological catheter examination was performed. A diagnosis of Taussig-Bing syndrome was made.
The infant developed heart failure, along with pneumonia, and died 43 days after birth. Autopsy revealed heart anomaly, hemorrhagic pneumonia and congested liver.
In general, Taussig-Bing syndrome is a rare case of cardiac anomaly and we have been unable to find a previous report similar to the present case.

View full abstract

A case of diabetic coma associated with acute renal tubular necrosis is reported.
The patient was a 24-yr-old man. He had suffered from a common cold 2 weeks beforeadmission. His complaints on admission were abdominal pain, thirst, polyuria and weightloss. Hyperglycemia (1, 005 mg/dl) and acetonuria with metabolic acidosis (pH 7.1) indicated diabetic ketoacidosis. Continuous intravenous infusion of insulin (4 unit/hr) was begun immediately. However, he became oliguric and markedly edematous. Acute renal failure accompanied by severe hypermyoglobulinemia (23, 680 ng/ml) and a transient DIC (platelets 2.3 x 104/mm3, serum FDP 40 mg/dl) probably resulted from acute renal tubular necrosis, which was demonstrated by renal biopsy and spontaneously relieved after the performance of the 21st hemodialysis. The severe hypermyoglobulinemia may have derived not only from the ketoacidosis itself and circulatory disturbance, but also from direct invasion of viruses into the muscle tissues. This may represent a major factor contributory to the acute renal tubular necrosis.

View full abstract

Today, the ultimate goal of diabetes care is to prevent the occurrence of diabetic complications or at least to reduce their severity. Data have been accumulated which indicate that the microangiopathy of diabetes is preventable by normalization or near-normalization of the metabolic disorders.
Continuous subcutaneous insulin infusion therapy (CSII) with a portable pump appears to represent one of the best therapies at present for type I diabetes. Since there have been only a few detailed reports on long-term trials of CSII, we attempted to treat two cases of type I diabetics by CSII.
Case 1 was a 33-yr-old insulin-dependent pregnant diabetic who had lost a baby 8 years previously by intrauterine fetal death at the 38th gestational week. Her diabetic control with conventional treatment became increasingly unsatisfactory in the 3rd trimester of her second pregnancy. At the 28th week of pregnancy, when her baby was endangered by fetal distress, CSII was introduced. Near-normal plasma glucose profiles were obtained, and urinary sugar and ketone bodies in the blood decreased markedly. The function of the fetoplacental unit also improved. CSII was continued for 58 days to the day of delivery, and she delivered a healthy boy weighing 2, 980 g without complications.
Case 2 was a 51-yr-old female, typical brittle diabetic with frequent attacks of insulin-induced hypoglycemia. During a one-week admission for CSII, she was educated in how to use the portable pump. After her discharge, she regularly measured her blood glucose level with dextrostixr and reported the values to her doctor for medical assessment. She has never experienced hypoglycemic coma, except for a few mild insulin reactions for 6 months at home. Near-normal fasting plasma
glucose and HbAI levels were achieved. During CSII, there were no problems with the batteries, pump or injection sites.
The clinical courses of the two above cases suggest that CSII can be useful for maintaining strict control of blood sugar levels in diabetics, especially in brittle or pregnant diabetics. Although several technical problems remain to be solved, it is concluded from the present observations that long-term CSII is available in its present form.

View full abstract

A 43-year-old male patient was admitted to our hospital with the chief complaint of leg malaise on 5 Sept. 1977. He had not been able to stand up by himself for 2 days prior to admission. Laboratory studies revealed serum potassium 1.4 mEq/l, CPK 2, 475 u, GOT 149 u, GPT 69 u, LDH 568 W.u., γ GTP 157 u, and aldolase 13.4 u. The activity of serum CPK returned to within normal limits as the muscle weakness improved. The serum potassium level, however, was 2.6 mEq/l even at the highest level probably due to 2-4 bouts/day of continuous watery diarrhea. An electrocardiogram revealed no signs of acute myocardial infarction.
The muscle weakness in this case was presumed to be due to hypopotassemia, which was in turn due to continuous diarrhea. The diarrhea in this case was thought to be diabetic diarrhea. The high activity of serum CPK was considered to result from the hypopotassemia and subsequent muscle weakness. The sigmoid colon revealed patterns of Kerckring's folds and a thumb-print like image on barium enema examination. The mucosal surface of the sigmoid colon and rectum demonstrated edema and soft polypoid lesions on colonofiberscopy. The biopsied mucosa showed minimal fibrosis and slight edema in the mucosa proper. The histological findings for biopsied jejunal mucosa were thought to be normal according to several reports. However, almost no reports have involved barium enema, endoscopic and histological examinations of the colon. Further studies are required to clarify whether the findings in the present case are specific to this disease entity or not.

View full abstract

It is well known that glycosylated hemoglobin, designated as hemoglobin AI (HbAI), can provide useful information regarding logn-term blood glucose control in diabetic patients.
It is well known that glycosylated hemoglobin, designated as hemoglobin AI (HbAI), can provide useful information regarding logn-term blood glucose control in diabetic patients.
Red blood cells from normal adults were incubated in a medium with a high-glucose concentration. The HbAIc concentration showed an increase of 141% at 7 days and 146% at 9 days after incubation compared to the starting level. After 7 days of incubation, the red blood cells were transferred to the medium without glucose and incubated for a further 2 days. The concentration of HbAIc decreased rapidly, reaching 114% compared to the starting level after 2 days.
The above findings indicate that part of HbAI forms an unstable linkage as well as a Schiff base compound and fluctuates with rapid changes in blood glucose concentration. Clearly, detailed observations for rapid changes of HbAI concentration should be made in the future.

View full abstract