The following parameters were measured in 60 diabetic patients: MCV (motor conduction velocity), TL (terminal latency), SCV (sensory conduction velocity) and NAP (nerve action potential) of the median nerve.
Stimulus (150 V, 0.2 ms) was applied to the 2nd finger using ring electrodes. Needle electrodes (interelectrode distance 3 cm, bipolar lead) were employed as the recording electrodes. NAP's were recorded from the wrist and elbow. Each potential was added 20 times using a computer. SCV's were measured from the 2nd finger to wrist and from the wrist to elbow. The MCV (from elbow to wrist) and TL were also measured.
The SCV, NAP and MCV values were decreased in diabetics compared to healthy controls. No close relationship existed between nerve conduction and the duration of diabetes mellitus, method of. therapy (diet and oral diabetic drugs) or age. The SCV values were more decreased in poorly controlled diabetics.
SCV and NAP were more significantly reduced in diabetics in the 3rd stage (Scott's classification), with paresthesia, decreased vibratory sensation and diminished light touch, than in those who did not complain of such manifestations. SCV and NAP were also significantly reduced in diabetics with loss of patellar and or Achilles jerk.
On the basis of the above findings, it is concluded that the onset of peripheral nerve involvementcan be prevented if diabetes mellitus is more or less well controlled, and that some relationship exists between diabetic peripheral polyneuropathy and retinopathy, which is considered representative of microangiopathy.

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Rat pancreatic islets isolated by the collagenase method were cultured for 14 days in modified TCM 199 containing 5.6 mM glucose, 5.6 mM glucose plus 1 mM adenosine, 16.7 mM glucose, and 16.7 mM glucose plus 1 mM adenosine.
The post-cultured islets were challenged with 10 mM arginine, 10 mM leucine, and either of these amino acids in the presence of 8.3 mM glucose during a 60 min incubation. The insulin release was then compared.
Islets cultured in media of all types except the 5.6 mM glucose medium preserved adequate8.3 mM glucose-induced insulin release. They showed increased insulin release by arginine and leucine with or without glucose. The insulin secretory response to leucine was more marked than that to arginine in the absence of glucose, while the presence of glucose caused a greater increase in insulin response to arginine than to leucine.
Islets cultured in 16.7 mM glucose and 16.7 mM glucose plus 1 mM adenosine demonstrated greater insulin secretory response to arginine than those cultured in 5.6 mM glucose plus 1 mM adenosine, whereas leucine-induced insulin release was similar among all islet cultures on these different kinds of media.
The above findings suggest that adenosine may be a useful agent in maintaining the function of long-term cultured islets due to preservation of the insulin response to physiological stimuli such as glucose and amino acids. They also suggest, in relation to insulin release, that arginine may act mainly as a potentiator which enhances insulin release by a primary stimulus or stimulator, while leucine acts as a stimulator.

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An immunochemical method was developed to measure two different triglyceride lipase activities in rat postheparin plasma: hepatic triglyceride lipase (H-TGL) and extrahepatic lipoprotein lipase (LPL). The two lipases were separated by affinity chromatography using Sepharose covalently linked heparin. The H-TGL thus separated and partially purified was injected into a rabbit and the antiserum against this enzyme was produced. Use of this antiserum then permitted specific measurement of the two lipases in whole postheparin plasma. Although the exact roles of the two lipases in lipoprotein metabolism have not yet elucidated, the present method appears to represent an important technique for studying the pathogenesis of experimental hypertriglyceridemia.

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Only a few cases of type 3 hyperlipoproteinemia secondary to diabetes have been documented in Japan.
Three cases of diabetic coma which developed type 3 hyperlipoproteinemia are reported here.
Case 1: A 21-yr-old female was admitted due to diabetic ketoacidosis. On admission, her serum cholesterol and triglyceride levels were 332 mg/dl and 226 mg/dl, respectively. Agarose gel electrophoresis of serum lipoproteins showed a broad-β pattern. The VLDL (d<1.006) obtained by ultracentrifugation according to the method of Havel showed a floating-β band on agarosegel electrophoresis. VLDL-cholesterol was 57 mg/dl and the cholesterol/triglyceride ratio in the VLDL was 0.50. These data met the criteria for diagnosis of type 3 hyperlipoproteinemia. After treatment of the diabetic ketoacidosis, serum lipids and VLDL returned to normal levels and the VLDL showed normal pre-β mobility on electrophoresis. However, 2 weeks later, the VLDL showed a late-pre-β band, suggesting type 3 hyperlipoproteinemia. One month after the onset of diabetic ketoacidosis, hepatic triglyceride lipase activity was decreased to the level of 3.36 μEq FFA/ml/hr (normal: 9.20±3.70), while the extra-hepatic triglyceride lipase activity (4.33 μEq FFA/ml/hr) was slightly high (normal: 2.32±1.41).
Case 2: An 18-yr-old female was admitted due to diabetic ketoacidosis. On admission, her serum cholesterol and triglyceride levels were 367 mg/dl and 255 mg/dl, respectively. Agarose gel electrophoresis of serum lipoproteins showed a broad-β band which consisted of two bands migrating between β and pre-β bands. After treatment of the diabetic ketoacidosis, the electrophoretic pattern changed from type 3 to 2b and then to 2a.
Case 3: A 62-yr-old man was admitted due to hyperosmolar nonketotic diabetic coma. On admission, his serum cholesterol and triglyceride levels were 177 mg/dl and 406 mg/dl, respectively. Agarose gel electrophoresis of serum lipoproteins showed a broad-β band. After treatment of the diabetic coma, the electrophoretic pattern changed from type 3 to 4 and then to 2a. One month before the onset of diabetic coma, hepatic triglyceride lipase activity was decreased to the level of 3.23 μEq FFA/ml/hr, while extra-hepatic triglyceride lipase activity was normal (1.63μEq FFA/ml/hr), and the VLDL showed a late-pre-β band on electrophoresis.
These results indicate that deficiency of lipoprotein lipase activity, especially of hepatic triglyceride lipase activity, might play some role in the pathogenesis of type 3 hyperlipoproteinemia.

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A patient who had shown generalized allergic skin reactions to conventional insulin was desensitized by Monocomponent Insulin injections. At the first stage, this diabetic could not receive conventional insulin treatment due to allergic reactions. After Monocomponent Insulin had been increased to the largest dose without any such reactions, conversion of treatment from Monocomponent to conventional insulin induced urticaria. Such skin reactions continued even after readministration of Monocomponent Insulin. Decreasing the dose of insulin was then attempted, and under this clinical course, the urticaria disappeared and good control of the patient's diabetes mellitus was established.
Serum insulin binding antibody (IgG) increased gradually during the course of desensitization.The Prausnitz-Küstner test and skin reactions to insulin were positive even after desensitization. On the basis of these findings, it is suggested that antibodies belonging to IgG might be blocking antibodies. However, before the increase of IgG antibody was found in the patient's serum, desensitization was almost completed. This suggests the possible existence of another mechanism ofdesensitization, such as neutralisation of sensitizing antibody.

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Factitious hypoglycemia was suspected in an insulin-dependent 13-yr-old female diabetic, who experienced repeated episodes of “spontaneous” hypoglycemia. The patient confessed to surreptitious administration of insulin before she was admitted.
The level of insulin which was extracted from the patient's serum was markedly increased during the hypoglycemic periods, and decreased with cessation of insulin administration.
The fact that human C-peptide was not elevated in response to stimulation with intravenous glucose and tolbutamide indicated that the extracted insulin was not endogenous.
This is the first case of factitious hypoglycemia reported in Japan.

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A preliminary study of the clinical application of enzyme-immunoassay (EIA) for insulin is reported. The insulin ETA kit, using the sandwich method with anti-insulin serum sensitized plastic beads as the solid phase and horseradish peroxidase as the labeling enzyme, was kindly supplied by Mochida Pharmaceutical Co. (Tokyo, Japan). The kit had a working range of 5 to 320 μU/m/ and gave good reproducibility. Blood samples were taken from 47 patients ((I) 20 diabetics treated with diet alone, (II) 10 diabetics treated with sulfonylurea oral hypoglycemic compounds, and (III) 17 non-diabetics) given 50 g-OGTT. The samples were analyzed for serum insulin by EIA and radioimmunoassay (RIA). The correlation coefficients between the values determined by RIA (X) and EIA (Y) were;(I) r=0.93, (II) r=0.78, (III) r=0.92, and for the total samples, r=0.91. A regression equation of Y=0.872 X+3.51 μU/m/ was obtained. ETA obviates the disadvantages associated with the measurement and handling of radioisotopes in RIA, and expensive equipment is not required. Based on the above findings, the insulin ETA kit is recommended for routine analysis of serum insulin.

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