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Several factors indicate that autoimmune mechanisms may play a part in the aetiology of insulin-dependent diabetes mellitus. At the onset of the disease in 10 children (aged 11-16 years) plasmapheresis was performed four times over one to two weeks. Seventeen age-matched children with the same clinical features served as controls. The C-peptide concentrations at onset were the same in the two groups, but after one month the children treated with plasmapheresis had significantly higher values. This difference became even more pronounced after three, nine, and 18 months, both during fasting and at the maximum response to a standardised meal. The study group also had a significantly more stable metabolism, longer partial remission, and no higher insulin requirement. Of the 10 treated children islet-cell cytoplasmic antibodies were present in seven before plasmapheresis and in nine during treatment. The antibodies remained detectable in five and six out of nine patients at one and six months respectively after plasmapheresis. Although the mechanisms are obscure, plasmapheresis performed at the onset of insulindependent diabetes mellitus may help to preserve betacell function.

Summary. Kidney function was studied in six normal males before and during a 2 h glucagon (10ng/kg/min) infusion. The following variables were determined during each 20 min clearance period; glomerular filtration rate (GFR), renal plasma-flow (RPF), filtration fraction (FF), urinary albumin and/32-microglobulin-excretion rates. Glucagon infusion resulted in a fourfold increase in plasma glucagon concentration. The infusion induced a significant increase in GFR (+9%), FF (+ 9%) and urinary fl2-microglobulin excretion rate (+ 32%), (p < 0.01). RPF and urinary albumin excretion rates were not significantly changed. We suggest that glucagon may contribute to the reversible kidney function alterations typically found in poorly regulated juvenile diabetes, a state with relative or absolute hyperglucagonaemia.

Plasma glucose and pancreatic-glucagon-like immunoreactivity (GLI) were measured in normal subjects and in patients with chronic pancreatitis after an intravenous insulin injection. Both groups showed a fall of about 40 mg/100 ml in plasma glucose at from 0 to 30 minutes. In the normal group, the pancreatic GLI increased significantly above the 0-value at 30 and 60 minutes. No increase was observed in the pancreatitis patients. In all cases a decrease in gut GLI was observed during the test.

Oral glucose tolerance tests (1.75 g glucose/ kg ideal body weight) were performed in 29 normal subjects, 17 maturity-onset diabetics (D I) and 8 juvenile type diabetics (D II). Glucose, IRI, pancreatic and gut ghcagon-like immunoreactivity (GLI) were determined at various intervals. The basal levels of pancreatic GLI in the three groups were as follows: normals: 0.33 :~ 0.03; D I: 0.43-u0.06; and D II: 0.50-t-0.05 ng equiv./m1 (mean • s.e.m.). After glucose, a significant decrease in pancreatic GLI was observed in the normals, whereas the diabetics showed no significant change. An increase in gut GLI was observed in all persons. The importance of the GLI levels and variations is discussed.

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ABSTRACT. Ludvigsson, J., Johannesson, G., Heding, L., Häger, A. and Larsson, Y. (Departments of Paediatrics and Neurophysiology, University Hospital Linköping, Sweden and Novo Research Institute, Bagsvaerd, Denmark). Sensory nerve conduction velocity and vibratory sensibility in juvenile diabetics. Relationship to endogenous insulin. Acta Paediatr Scand, 68: 739, 1979.—Sensory nerve conduction velocity (NCV) and the vibratory sense (biothesiometry) were determined in 67 children and adolescents with insulin dependent diabetes. Age at onset of diabetes varied between 1–14 years (mean ±S.D. 6.5±3.6) and the duration of diabetes between 4–17 years (7.7±3.4). Within ±3 months of the nerve function tests blood was drawn for determination of C‐peptide and insulin antibodies (IgG and IRI). A low NCV (<50 m/s) in the sural nerve and/or an abnormal vibratory sense (≥1.0 microns) were found in 34 patients (50.7%). Measurable fasting serum C‐peptide 0.04–0.60 pmol/ml (0.17±0.15) was found in 16 patients (23.9%). All but one patients had insulin antibodies with IgG 0.130–11.029 mU/ml (2.957±2.509) and total IRI 10–9120 μU/ml (1204±1723). In multiple regression analysis we did not find any correlation between nerve function and sex, age, or age at onset of diabetes, and there was only a weak relationship between NCV and duration. However, there was a positive correlation between NCV and C‐peptide (p<0.001). Vibration sense was also better among patients with C‐peptide (p<0.05). The results support the view that insulin deficiency contributes to peripheral diabetic neuropathy.