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J A Lutterman

Publications and source records attributed to J A Lutterman.

67 records · Page 4Linked to original sources
PubMed1986

Non-specific binding of insulin in an equilibrium binding assay of insulin antibodies.

In liquid phase assays for insulin binding antibodies (IBA), total binding of insulin is composed of specific and non-specific binding (NSB). Sometimes NSB is determined in serum of healthy individuals and then subtracted from total binding of IBA positive serum to obtain specific binding. This method does not take into account that NSB might vary from plasma to plasma. This possibility was investigated by means of a computerised non-linear curve fitting routine for the evaluation of measurement results of an (equilibrium) binding assay for IBA, which yields estimates of NSB for each plasma individually. From each of 19 insulin treated diabetic patients, 4 blood samples, taken at different points in time, were available for IBA and NSB measurement. It was found that inter-patient variance of NSB exceeded within-patient variance (p less than 0.01) and, in a number of instances, within-patient variance was greater than experimental variance. Our results indicate that it is advisable to use methods of IBA evaluation that take these NSB variations into account.

Antibodies↗
PubMed1982

Apolipoprotein C in type 2 (non-insulin-dependent) diabetic patients with hypertriglyceridaemia.

The composition of apolipoprotein C of the very low density lipoproteins (VLDL) was examined in 23 treated Type 2 (non-insulin-dependent) diabetic patients, who had elevated VLDL concentrations. Apolipoprotein C was separated by isoelectric focussing into apolipoprotein C-II which is known as the specific activator of lipoprotein lipase, and three apolipoprotein C-III fragments. A regulatory role has been ascribed to the ratio of apolipoprotein C-II to apolipoprotein C-III in the removal of plasma triglycerides. In our diabetic group, the composition of apolipoprotein C of the VLDL particles was not different from that of a healthy control group. In particular, the above apolipoprotein ratio and the relative amounts of apolipoprotein C-III fragments were normal. Hypertriglyceridaemia in these diabetic subjects does not seem to be related to alterations in the apolipoprotein C composition.

Apolipoprotein C-I↗
PubMed1981

The relationship between residual insulin secretion and metabolic stability in type 1 (insulin dependent) diabetes.

The purpose of this study was to investigate whether the great differences in metabolic control between labile and stable insulin dependent juvenile diabetics could be explained by differences in residual pancreatic B cell function. Nine labile diabetics, ten stable diabetics on one insulin injection a day and nine stable diabetics on two insulin injections a day were investigated during a 24-h period during which they maintained their usual diet and insulin therapy. Serum C-peptide concentrations were measured after removal of proinsulin bound to insulin antibodies. The labile diabetics did not show any significant change in C-peptide concentrations despite great fluctuations in plasma glucose concentrations. In six patients with stable diabetes, C-peptide responses after the main meals could be demonstrated and there was a significant correlation between the concentrations of C-peptide and glucose (r = 0.85, p less than 0.001). The other stable patients, having the same mean plasma glucose concentration and mean amplitude of glycaemic excursions, did not show any C-peptide response. It is concluded that persistent insulin secretion is not a prerequisite for metabolic stability. Severe lability, however, seems to occur only in the absence of residual insulin secretion.

Adult↗
PubMed1981

Combined deficiency of apolipoprotein C-II and lipoprotein lipase in familial hyperchylomicronemia.

The underlying pathophysiological defect was studied in four siblings with familial hyperchylomicronemia. Deficiency of apolipoprotein C-II and E-3 was identified. In addition, these subjects had markedly decreased LPL activity in postheparin plasma. Addition of normal plasma to the assay as source for apoC-II enhanced LPL activity only to a limited extent. In contrast with previously reported patients with apoC-II deficiency, a far less pronounced effect of intravenous infusion of normal plasma was seen in one of the siblings, probably due to the combined deficiency of apoC-II and LPL. Plasma VLDL-TG turnover rate was not decreased in one of the siblings with apoC-II and LPL deficiency, suggesting different metabolic pathways for chylomicrons and VLDL. Family study confirmed an autosomal recessive mode of inheritance both for apoC-II and for apoE-3 deficiency. The mode of inheritance for LPL deficiency could not be established exactly.

Adult↗
PubMed1979

Treatment of severe diabetic ketoacidosis. A comparative study of two methods.

Patients with severe diabetic ketoacidosis (pH less than 7.10) were treated according to two protocols. Protocol I consisted of high-dose insulin therapy by intravenous and intramuscular injections and bicarbonate infusion and was used in the first 12 patients; they received an average of 260 U insulin and 167 mmol bicarbonate in the first 6 h of treatment. Protocol II consisted of low-dose continuous intravenous insulin therapy, 8 U/hour, without bicarbonate in a further 12 patients. Rehydration and potassium-supplementation were the same in both methods. Basal data of both groups were not significantly different. The fall of plasma glucose concentration, rise in arterial pH and decrease in 3-hydroxybutyrate were similar in the two groups. The mean time to achieve a pH equal to or greater than 7.30 was 6.8 hours in the high-dose group and 7.6 hours in the low-dose group (p greater than 0.10). Potassium supplementation and potassium concentration during both treatments were the same. During the low-dose treatment the mean (+/- SD) plasma insulin concentration was 121 +/- 46 microU/ml. The presence of insulin binding antibodies did not result in lower free insulin concentrations. Thus, in the treatment of severe ketoacidosis continuous intravenous therapy with low-dose insulin is as effective as high-dose therapy and bicarbonate-administration is probably unnecessary.

Adult↗
PubMedDate not supplied

Plasma lipoproteins, apolipoproteins, and triglyceride metabolism in familial hypertriglyceridemia.

Several parameters of lipoprotein metabolism were examined in 38 men with primary hypertriglyceridemia (phenotype IV). Family investigation showed that 17 men had familial combined hyperlipidemia (FCH), seven had familial hypertriglyceridemia (FHT), and 14 had unclassified hypertriglyceridemia (UNC). In all three groups, plasma high density lipoprotein (HDL) cholesterol and the concentrations of apolipoprotein A-I and A-II were decreased, and apolipoprotein B was increased, each to the same extent. These results are compatible with an increased risk of cardiovascular disease in both FCH and FHT patients. The mean concentration of LDL cholesterol and the ratio of LDL to HDL cholesterol were significantly higher in FCH subjects, which could explain their increased risk. Postheparin lipoprotein lipase and hepatic lipase were the same in both groups. Determination of apolipoprotein C composition, which may modulate lipoprotein lipase activity, did not reveal any abnormalities in the different groups. In both FCH and FHT, the mean turnover rate of plasma triglycerides was almost twice normal, indicating that overproduction of plasma triglyceride plays an important role in both disorders. However, there was an overlap with normal controls, indicating impaired triglyceride removal in some subjects. The underlying mechanism of hypertriglyceridemia in FCH and FHT therefore seems to be heterogeneous.

Aged↗
PubMedDate not supplied

Comparison of efficacy of human and porcine insulin in treatment of diabetic ketoacidosis.

The efficacy of semisynthetic human insulin (HI) and monocomponent porcine insulin (PI) in treatment of diabetic ketoacidosis (DKA) was compared in 10 (PI) and 11 (HI) patients in a double-blind randomized study. Insulin (8 U/h i.v.), fluid replacement (0.65% NaCl and 5% glucose), and KCl supplements were administered according to a fixed protocol. Glucose, potassium, sodium, creatinine, calcium, phosphate, and free-insulin concentrations were never significantly different during the study. At the start, mean +/- SD of pH was 7.10 +/- 0.14 in the HI group and 7.10 +/- 0.12 in the PI group. The time to reach arbitrary values for pH, bicarbonate, base excess, and beta-hydroxybutyrate was shorter during HI treatment, but the differences were not statistically significant. During HI treatment, the arbitrary value of 1.0 mM of acetoacetate was reached faster than during PI treatment (5.2 +/- 2.6 and 8.4 +/- 0.9 h, respectively; P less than .05). The concentration of acetoacetate was significantly different between the two groups after 6 and 7 h of insulin treatment (6 h: HI 0.82 +/- 0.50 mM and PI 2.19 +/- 1.65 mM, P less than .05; 7 h: HI 0.51 +/- 0.40 mM and PI 1.74 +/- 1.54 mM, P = .05). We conclude that recovery from DKA during treatment with HI might be slightly faster than during treatment with PI. If this difference is real, it does not seem clinically important.

3-Hydroxybutyric Acid↗
PubMedDate not supplied

Performance of subcutaneously implanted glucose sensors: a review.

Despite a considerable amount of research attributed to the development of an implantable glucose sensor, to date there is no clinically applicable concept for continuous glucose monitoring. Investigations to validate the subcutaneous tissue for continuous glucose sensing mostly comprise short-term implantations of glucose sensors. Most implanted glucose sensors showed a significant decay in sensitivity over the implantation period. This bioinstability was not to be expected from the in vitro performance of the sensors. In this article, the influence of possible failure mechanisms on the poor in vivo performance of subcutaneously implanted glucose sensors is reviewed.

Animals↗