A method for the classification of two types of diabetes mellitus (DM), type I and type II, was attempted based on the scoring of certain clinical signs. In total, 161 diabetics who had experienced onset of DM at ages of less than 35 years old, were judged as type I-DM or type II-DM by seven diabetologists. After the systematic errors of the clinical signs in both types had been analyzed statistically, the type I indices (TII) which represent the features of type I-DM were calculated. The respective TII values, were as follows: 1) age at discovery of DM: less than 15y.o., +7; 16-30 y.o., -1; more than 31 y.o., -4; 2) clinical symptoms at discovery of DM: presence, +3; absence, -5; 3) family history of DM within the second degree of consanguinity: absence, +3; presence, -4; 4) initial treatment within 6 months after discovery of DM: insulin administered, +9; not administered, -5; 5) past history of ketouria: presence, +9; absence, -6; 6) present obesity index (%): less than 85%, +6; 85-100%, +1; 100-115%, -2; more than 115%, -5; 7) present control of blood glucose level: poor, +4; good or fair, -3; and 8) present requirement of insulin (units/kg body weight/day): more than 0.45, +10; 0.30-0.45, +7; 0.15-0.30, -3; less than 0.15, -9.
The sum total for TIT (ΣTII) involving the above 8 signs was calculated in all cases. By statistical analysis, ΣTII values of more than +6 and less than -12 were classified as type I and type II, respectively. This scoring is expected to be useful as an objective classification of DM, since the precision in diagnosis using the method proved satisfactory.

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The present study was undertaken to determine the amount of fecal bile acid excretion in 26 diabetic subjects. The subjects were divided into 3 groups according to the presence of diabetic neuropathy. Group I included 13 cases without neuropathy, Group II included 11 cases with diabetic neuropathy, and Group III included cases with diabetic diarrhea. Fecal bile acid and fecal fatty acid were determined by gas-liquid chromatography. The following results were obtained.
1) The fecal wet weight per day was 141.8g in controls, 185.0g in Group I, 238.5g in Group II, and 280 and 700g in Group III.There was no significant difference among the groups.
2) The fecal bile acid excretion per day was 4.56mg/kg in controls, 6.89mg/kg in Group I, 15.0mg/kg in Group II, and 15.2 and 24.7mg/kg in Group III.The fecal bile acid output was significantly increased in Group II compared to the controls and Group I.
3) The ratio of primary bile acid to total bile acid was 14% in controls, 13.7% in Group I, and 27.6% in Group II.The ratio was markedly increased in the2cases of Group III with diabetic diarrhea (40.8%and76.5%).
4) Increased fecal fatty acid excretion (steatorrhea) was present in only one case of Group I and Group II, and the increase was to a slight degree.
The above reslts suggest that fecal bile acid excretion was increased in diabetics with neuropathy and with diabetic diarrhea, but was not increased in diabetics without neuropathy compared to controls.

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In order to elucidate the influence of diabetes mellitus on osteopenia, the bone mineral content at midradius (radial mineral content, RMC) was measured by photon absorptiometry in 90 patients with diabetes mellitus (32 IDDM, 58 NIDDM) and 65 normal controls.
It was suggested that there were different pathogenetic factors of bone mineral loss between ID DM and NIDDM.
In IDDM, the RMC was inversely correlated to the duration of diabetes (p<0.05) and to mean fasting blood glucose (p<0.05) and also diminished significantly in patients with proliferative diabetic retinopathy and/or severe neuropathy Moreover, the RMC was also significantly lower in IDDM withMOnckeberg's medial arteriosclerosis as compared to those without these findings (p<0.05).
In NIDDM, on the other hand, there was no significant correlation with any of these clinical features of diabetes.
The serum calcium, phosphorus, immunoreactive parathyroid hormone and alkaline phosphatase levels were all within normal range in all diabetics. However, the values of the urinary excretion rate of calcium correlated positively with the degree of hyperglycemia (p<0.01).
These results suggest that the bone mineral loss in patients with diabetes mellitus may be explained, in part, by the continued deterioration of metabolic control and/or the excess of urinary calcium excretion.

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In order to evaluate the significance of residual B-cell function in determining blood glucose instability in 24 insulintreated diabetic patients, the relation between serum C-peptide secretory capacity in response to 50 g oral glucose load and the standard deviation (SD) of the mean blood glucose (MBG) level or the M value obtained from the diurnal blood glucose curve was examined. The C-peptide immunoreactivity (CPR) of sera after polyethylene glycol precipitation (free-CPR) was assayed in determining the residual B-cell function. ¹²⁵I-insulin binding to insulin antibody in the patient's serum was determined by the ethanol precipitation method.
In all insulin-treated diabetic patients, fasting free-CPR, Σfree-CPR and free-CPR response (peakfasting free-CPR) during glucose load were 1.0±0.1 (M±SE), 7.1±0.9 and 0.8±0.1 ng/ml, respectively. The SD of the MBG level and M value were 59±4 mg/dl and 43.9±6.0, respectivey. No significant difference was noted in these values in the presence or absence of insulin antibody.
A significant negative correlation was observed between fasting free-CPR, Σfree-CPR or free-CPR response and the SD of the MBG level (p<O.01, p<O.01 and p<O.05, respectively). A similar significant negative correlation was noted between each parameter of free-CPR and the M value (p<O.05).
Patients with an M value of more than 43 (n=11) were significantly younger (p<0.05). their MBG levels and SD were significantly larger (p<0.01 and p<0.005, respectively) and fasting free-CPR, I free CPR and free-CPR response were significantly lower (p<0.05, p<0.01 and p<0.05, respectively) than those in patients with an M value of within 43 (n =13).
There was no significant correlation between either the SD of the MBG level or the M value and ¹²⁵I-insulin binding in patients with insulin antibody.
These results suggest that instability of blood glucose depends upon the residual B-cell secretory capacity, but not the presence of insulin antibody.

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100 g oral glucose tolerace test (OGTT) was performed in 53 insulin-treated diabetics. Those with a body weight index>110%, abnormal liver function or serum creatinine concentration>1.4 mg/dl were excluded from the study. The sera were treated with polyethylene glycol before assay to remove proinsulin-insulin antibody complex in insulin-treated diabetics. The same method was also applied to the sera obtained from 36 non-insulin-treated diabetics for comparison.
The patients were divided into four classes according to the sum of blood glucose values during the OGTT as follows:≤1100 mg/dl (Class 1), 1101-1500 mg/dl (Class 2), 1501-1900 mg/dl (Class 3) and ≥1901 mg/dl (Class 4). We found significantly lower Σ serum free CPR values (the sum of serum free C-peptide immunoreactivities during the OGTT) in insulin-treated patients when compared with non-insulin-treated patients in all groups except Class 1, in which the number of patients was too small to allow a comparison. The coefficients of variation of fasting blood glucose values (C.V. of FBG, N=10) were significantly higher in insulin-treated patients as compared with non-insulin-treated patients in Classes 2 and 3, although there was no statistical difference of mean FBG between them. the C.V. of FBG was inversely correlated to Σ serum free CPR values in insulin-treated diabetics (r=-0.47, p<0.001).
Thus, residual B-cell secretory capacity in insulin-treated diabetics is lower than in non-insulintreated diabetics and inversely correlated to the instability of fasting blood glucose values.

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In order to investigate serial changes of blood pressure and the renin-angiotensin-aldosterone system in diabetes mellitus complicated by hypertension, the blood pressure, renin and aldosterone in diabetic spontaneously hypertensive rats (SHR) induced by streptozotocin were evaluated for 25 weeks. Female SHR (8 weeks old, n=60) were injected with streptozotocin (45 mg/kg) via a tail vein. These SHR were divided into three groups as follows: Group I: diabetic SHR (n=31), Group II: temporary hyperglycemic SHR (n=9), and Group III: non-diabetic SHR (n=14). The serial changes of blood pressure in each group and control SHR (n=25) were evaluated. 5 diabetic SHR of group I were treated with insulin from the 10th week to 15th week and the changes in blood pressure were studied. Furthermore, the changes of plasma renin activity (PRA) and plasma aldosterone concentration (PAC) in group I and the controls were evaluated.
(1) Serial changes of blood pressure (mmHg)
Group I showed elevation of blood pressure during the first 7 weeks as in the controls, but there was a significant reduction (p<O.001) of blood pressure over the 8th week compared with the controls. The reduced blood pressure in group I was not increased by insulin therapy. Group II showed a significant reduction (p<O.001) of blood pressure at 8 weeks, but there was no significant change over the 10th week compared with the controls. Group III showed no significant change compared with the controls.
(2) Serial changes of PRA (ng/ml/h) and PAC (ng/dl)
Group I showed a slight decrement of PRA at 4 and 7 weeks, and a significant decrement (p<0.05) of PRA at 13 and 25 weeks compared with the controls. Group I showed a slight increment of PAC at 4 and 7 weeks, a slight decrement of PAC at 13 weeks, and a significant decrement (p<0.01) of PAC at 25 weeks compared with the controls.
It is concluded that decrement of aldosterone secondary to decrement of renin can cause reduction of blood pressure in diabetes mellitus complicated by hypertension.

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To examine the ideal state for medical practice and treatment ofdiabetes, we carried out an identical investigation to that which had been made by questionnaire ten years ago.In the present study, 605 hospitals all over the country that were concerned with diabetes mellitus and 398 Lay Societies belonging to JDLS (the Japan Diabetic Lay Society) were selected.Most of the data obtained were compared with those of ten years ago.
The changes which had taken place during the past ten years included an increase in the number of hospitals with particular wards or rooms for patient education, an increase in the average number of times per month that patient education for diabetes was practiced at the hospitals, an increase in the average number of times per week that they had diabetes clinics for outpatients, and a marked decrease in the average number of diabetics that were treated by a single doctor in large clinics such as in university hospitals.However, it was found that one doctor had a large number of diabetic patients in small private or public clinics.The number of Lay Societies belonging to JDLS had increased remarkably, while the membership of the individual Lay Societies had decreased over the past ten years.
In Lay Societies of small scale, especially in small private orpublic clinics, it has proved difficult to practice particular patient education.For this reason, many have expressed the view that they hope to make the Lay Society a community circle.
Based on the above results, it can be said that there have beenmany desirable changes in the medical practice and treatment of diabetes, while the smaller inscale both the clinics and Lay Societies are, the more problems tend to arise for discussion.The authors therefore suggest as an important problem that we must discuss how to guide and organize both clinics and Lay Societies of small scale in the medical practice and treatment of diabetes.

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Both the islet cell cytoplasmic and cell surface antibodies (ICA and ICSA) were studied from the onset of diabetes to remission. A 24-year-old man was admitted to hospital on September 25, 1981, because of ketoacidotic hyperglycemic precoma.He had no history of diabetes. On admission, his blood glucose was 644mg/dl and blood gas analysis showed the following: pH 7.166, BE-23.6 mEq/l, Ht 52.5%.Continous subcutaneous insulin infusion was performed for a couple of days and then changed to NPH-insulin injection.
The dose of insulin was gradually decreased and on the 45th day after onset, an oral hypoglycemic agent was substituted for insulin.He was followed up as an out-patient and his disease was controlled well by diet and the hypoglycemic agent.For a couple of months, his blood glucose levels were within the normal range and the urine sugar was 0.4 g/24 hr.He was well until the middle of January 1982, when he developed a general cold.A few days later, he was readmitted to hospital because of hyperglycemia and hepatitis.
Both ICA and ICSA had been observed during the course of his disease.ICA or IUSA were found independently of each other.However, ICSA, which was determined quantitatively by immunoassay using ¹²⁵I-protein A, closely paralleled the clinical profile.ICSA may thus represent a marker of islet B-cell damage during the diabetic period, and may also be a useful pardmeter for diabetic prognosis.

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The case of a 14-year-old female with acanthosis nigricans, hyperinsulinemia and mild glucose intolerance is reported. Her mother and brother also had hyperinsulinemia and glucose intolerance. The patient's fasting plasma insulin level was 160 μU/ml by radioimmuno assay, 158μU/ml by radioreceptor assay, and a decreased sensitivity to exogenous insulin was observed. The plasma levels of cortisol, glucagon and growth hormone were normal, and neither anti-insulin nor anti-insulin receptor antibody was detected in her plasma. The plasma proinsulin level was less than 10 % of the total insulin immunoreactivities, and the biological activity of her plasma insulin was normal. Scatchard analysis revealed a decreased insulin binding to the patient's erythrocytes due to a decrease in receptor capacity.
These findings suggest that the glucose intolerance in the patient was caused by a congenital insulin receptor defect corresponding to type A on the classification of Kahn et al.

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It has been reported that the level of serum HDL-cholesterol in diabetics is lower than in normal subjects and that of insulin-treated subjects is higher than before treatment with insulin. The increase in serum HDL-cholesterol in insulin-treated diabetics is thought to be due to an increse in lipoprotein lipase activity.
There have been few reports discussing the relationship between the level of serum HDL-cholesterol and tha t of serm insulin.In the present study, the relationship between these two parameters was therefore investigated in rats treated with a low dose of streptozotocin. Such rats demonstrated hyperinsulinemia probably due to insulin-producing tumor. There was, however, no relationship between the two above parameters.
Hyperinsulinemia itself is not thought to influence the level of serum HDL-cholesterol.

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